Take a moment to think about the last time when you had an injury you could see. Maybe it was a scratch or scrape on your arm or leg, or even a cut on your finger. You probably knew what would happen next. Once the bleeding was under control, you expected a scab to form, and maybe wondered if you’d end up with a scar. At the center of this healing process was a cell called a fibroblast. Fibroblasts are the most common type of cell found in connective tissue and they play an important role in healing wounds by secreting collagen proteins that repair tissue.  

But sometimes these fibroblasts become confused about what they should be doing, leading to a condition called fibrosis. Researchers don’t fully understand why fibrosis occurs, but it leads to organs or tissues developing excessive fibrous tissue, which can interfere with multiple organs like the lungs, heart, liver, skin, kidneys, and eyes - ultimately leading to loss of organ function. Inflammation or fibrosis play a role in several diseases, including lupus, cystic fibrosis and scleroderma. There are currently no FDA approved drugs that can halt the progression of fibrosis or reverse it, making it an essential area of focus for research. 

In this episode of Science Never Sleeps, we'll be discussing scleroderma and fibrosis, and research to find treatments and possible cures.

Guest Notes: Dr. Carol Feghali-Bostwick is a Distinguished University Professor in the Division of Rheumatology & Clinical Immunology at MUSC focusing on fibrosis encompassing disorders such as Systemic Sclerosis (SSc) and Idiopathic Pulmonary Fibrosis. In addition to research, Dr. Feghali-Bostwick ‘s efforts include mentoring of junior investigators in patient-oriented research and directing the Center for the Advancement, Retention, and Recruitment of Women (ARROW). She also serves as the Vice-Chair of the Board of Directors of the National Scleroderma Foundation. 

Show Reference Links:

Feghali-Bostwick Basic Research Lab at MUSC

National Scleroderma Foundation

What is Ideopathic Pulmonary Fibrosis? - National Heart, Lung, and Blood Institute

♪

From the Medical University of South Carolina,

this is Science Never Sleeps,

where we explore the science, people,

and stories behind the scenes

of biomedical research happening at MUSC.

I'm your host, Gwen Bouchie.

Take a moment to think about the last time

you had an injury you could see.

Maybe it was a scratch or a scrape on your arm or leg,

or even a cut on your finger.

You probably knew what would happen next.

Once the bleeding was under control,

you expected a scab to form

and maybe wondered if you'd end up with a scar.

At the center of this healing process

was a cell called a fibroblast.

Fibroblasts are the most common type of cell

found in connective tissue

and they play an important role in healing wounds

by secreting collagen proteins that repair tissue.

But sometimes these fibroblasts become confused

about what they should be doing,

leading to a condition called fibrosis.

Researchers don't fully understand

why fibrosis occurs,

but it leads to organs or tissues

developing excessive fibrous tissue,

which can interfere with multiple organs,

like lungs, heart, liver, skin,

kidneys, and eyes,

ultimately leading to loss of organ function.

Inflammation or fibrosis play a role in several diseases,

including lupus, cystic fibrosis,

and scleroderma.

There are currently no FDA-approved drugs

that can halt the progression of fibrosis or reverse it,

making it an essential area of focus for research.

In this episode of Science Never Sleeps,

Dr. Carol Feghali-Bostwick joins us to discuss

scleroderma and fibrosis,

and her research to find treatments and possible cures.

Dr. Feghali-Bostwick

is a distinguished university professor

in the division of Rheumatology and Clinical Immunology at MUSC,

and she's the Kitty Trask Holt and Smart State Endowed Chair.

Dr. Feghali-Bostwick's research interests

focus on fibrosis and accompanying disorders,

such as systemic sclerosis

and idiopathic pulmonary fibrosis.

In addition to research, her efforts include

mentoring junior investigators in patient-oriented research

and directing the Center for the Advancement,

Retention, and Recruitment of Women.

She also serves as the Vice Chair

of the Board of Directors

of the National Scleroderma Foundation.

Stay with us.

♪

Dr. Feghali-Bostwick, thank you so much

for joining us on Science Never Sleeps.

It's a pleasure to be here.

So let's start today by talking about,

"What is fibrosis?"

A simple way of thinking about fibrosis

is to think of the tissues that affect thickening.

So fibrosis is excess production

of what we call extracellular molecules,

such as, for example, collagen, a common one,

that a lot of people know what collagen is these days.

But when cells in the body start to make

too much of these molecules

and stop being able to break them down

and clear them to keep normal levels of them,

that's when fibrosis happens,

and as a result, whatever tissue or organ is affected

becomes thickened and stiff.

How many people are impacted by this disease?

Really a lot of people are impacted

because fibrosis can affect nearly any organ in the body,

and it is a fairly advanced complication

of many different diseases.

Dr. Thomas Wynn, who was at the NIH,

had reported at one point that fibrosis results

in 45 percent of deaths in the developed world,

so that's a significant number.

So you mentioned that fibrosis affects

many different types of organs.

What are some examples of those organs,

and how do we see fibrosis

when those organs are affected?

So fibrosis can affect different organs

and is a result of different diseases.

So for example, if you think of the lung,

fibrosis can affect the lung,

but it's not one disease.

The lung can be impacted by fibrosis

and diseases such as idiopathic pulmonary fibrosis

or systemic sclerosis, which we call scleroderma,

the diseases we study.

You can have fibrosis around the airways in the lung

in something as common as asthma,

but you could also have fibrosis in the kidneys.

For example, those who are diabetic

can have fibrosis in their kidneys.

You could have fibrosis in the liver

as a result of different things,

whether it's alcoholic liver disease

or hepatitis C-induced liver fibrosis.

So there are a lot of different causes

of fibrosis in each organ,

and the organ that is affected is usually affected

as a result of one of numerous diseases

that can cause fibrosis.

So as a researcher, does the fact

that fibrosis can affect different organs

make it more challenging to research,

or does it open up more opportunity

to understand what's happening?

That's a great question.

I would say probably both.

The challenges come from

finding mechanisms and pathways

that are abnormal in fibrosis

that are affected similarly in different organs,

so you can find a common or shared feature of fibrosis

in different organs.

So that's where some of the challenges are

in the research, leading to a better understanding

of what's happening in fibrosis, and what causes it,

and how can we change it and change the outcomes?

The opportunities are exactly the same.

If you find a pathway or a therapy

that affects mechanisms in more than one organ,

now you have something that's potentially of benefit

to so many people with so many different diseases.

We understand that fibrosis affects

a lot of different parts of the body,

so then I would imagine that makes treating it

quite complicated because of the different areas

where you would see it.

What are some of the more traditional

existing treatments for this?

We really don't have any

effective treatments for fibrosis.

We really don't have any FDA-approved drugs yet

that can either stop the progression of fibrosis

or reverse it.

So what's available out there that's FDA approved,

for example, for lung fibrosis

are treatments that slow down the progression of fibrosis.

The fibrosis continues, but at a much slower rate.

But really don't have anything out there

that we consider curative or reversing fibrosis.

So this makes this particular area of study

a really important one because there's

not much out there for patients who are experiencing this?

Exactly.

For your research specifically,

what type of fibrosis do you investigate?

What are you most interested in?

So my life has focused over the past

more than two decades

on studying fibrosis across two organs,

the lungs and the skin,

and the reason for that is one of the diseases we focus on

is systemic sclerosis,

also called scleroderma,

which is unique in that patients with scleroderma

can have fibrosis in multiple different organs.

So for example, individuals who have

hepatitis C-induced liver fibrosis

have fibrosis restricted to the liver.

Those who have asthma have fibrosis

restricted to the airways in the lungs.

But in scleroderma, the patients have

fibrosis of the skin, of the lungs, of the kidneys,

of the GI tract, of the heart,

so they have multiple organs affected.

As a result, we've been looking at two of those organs,

lungs and skin, because they're the more readily studied organs

compared to, for example, the GI tract for us,

because we figure if we can find

shared features of skin and lung fibrosis,

then those features are likely to also be relevant

for other organs, like the liver,

like the kidneys, like the GI tract,

like the heart.

So that's a space where some specialization

in looking at the specific organs

could have ramifications for other organs in the future,

rather than trying to do a lot of study

of a lot of different systems.

Exactly, so looking at fibrosis across organs

I think is critical so that we can identify

ways of improving the fibrosis

for patients with a variety of diseases,

and not be one disease centric or one organ centric.

I think it's interesting that we might hear about

some diseases that we don't realize

are linked to fibrosis.

So you mentioned scleroderma earlier,

but also in some of my research

I was reading about liver cirrhosis.

So we think about liver cirrhosis

and the things that that's connected to,

but the precursor to cirrhosis

is the fibrosis of the liver, correct?

Correct, cirrhosis and fibrosis.

Right, which really speaks to inflammation as well.

So many of the diseases where we see fibrosis

are linked to inflammation in the body.

So can you talk a little bit about

the role of inflammation in fibrosis

and how it impacts the patient?

In some of the diseases where fibrosis occurs

as the disease progresses or advances to later stages,

often the earlier phases of the disease

are characterized by inflammation.

So for example, in scleroderma

often patients have a lot of inflammation in their lungs

and that can be there for years

before they develop the more permanent fibrosis

that, once settled, usually is not resolved,

certainly not easily.

So often inflammation precedes fibrosis occurring.

Now inflammation has been a little bit controversial

in some of the diseases,

like idiopathic pulmonary fibrosis

there are sort of two camps in the field:

Those who believe inflammation occurs

and those who don't.

But there's a lot of scientific evidence

suggesting that some form of inflammation does happen

in the earlier phases of these diseases.

The fibrosis comes from a place

of the body trying to heal itself.

That's the mechanism that's being triggered.

But in the case of fibrosis, something goes wrong

and the healing happens too much,

and then it becomes a negative thing.

So the inflammation existing really is sort of

what the fibrosis is in response to, right?

We're triggering this healing mechanism

within the body that somehow goes awry.

You're absolutely right, and actually a lot of people

refer to fibrosis as uncontrolled wound healing,

because the mechanisms that occur in normal wound healing

or following injury of some sort,

not just injury to the skin,

but injury to the lung and other organs.

The organ starts to heal itself,

but something goes wrong and the healing process

becomes uncontrolled.

Actually many of the factors produced by the immune cells

that are involved in inflammation

are factors that we know experimentally in the lab

can trigger fibrosis in the cells that we study

and the models we study.

Things such as interleukin 6

that's made by the immune cells during inflammation,

or transforming growth factor beta,

we call it TGF-Beta, those we actually use in the lab

to trigger fibrosis in the cells.

So clearly the products,

what we call the hormones of the immune system

that are produced during inflammation,

are capable of initiating a fibrotic response.

So tell us a little bit more about the diseases

in the organs that you specifically study

and investigate in your research.

The primary disease that my lab focuses on

is systemic sclerosis or scleroderma

mostly because it is a prototypic disease.

As we discussed a little earlier,

in scleroderma multiple organs are affected,

so that makes it the ideal disease

to study fibrosis across organs.

But we also study other conditions,

like idiopathic pulmonary fibrosis,

that affects the lungs primarily,

because there are similarities

across diseases that have fibrosis in the same organ.

So scleroderma has fibrosis of the lungs.

IPF, idiopathic pulmonary fibrosis,

has fibrosis of the lungs, and although the fibrosis

is not 100 percent exactly the same,

there are similarities between the two diseases

and there are differences obviously as well.

Is scleroderma the same in everyone,

and whether it is or not,

does that make your research more challenging?

It is not the same in everyone.

It's actually very heterogeneous.

Scleroderma is very different,

and sometimes people say that no two patients are alike.

That's how different it can be.

The extent of involvement of the skin can vary a lot.

The rate of progression can vary a lot.

Which internal organ is affected can vary a lot.

Some people may have lung fibrosis, but not kidney.

Others may have kidney, but not lung fibrosis.

So it varies a lot from patient to patient

and we're trying to understand why that is.

In other words, is it dependent on what the trigger is

that says which form

or how severe your disease is going to be?

Is it susceptibility based on how prone you are to getting it

that determines that?

We do know that scleroderma is much more common

in women than in men.

However, when men get it they have a tendency

to have worse or more severe disease.

We also know that both Caucasians and African Americans

and Hispanics and other ethnicities

get scleroderma,

but the research has shown that African Americans

have more severe scleroderma than others,

so we're trying to understand that.

So one of the next steps in my lab

has been to try and understand,

in the setting of lung fibrosis in scleroderma,

what is the difference between the lung phenotype,

what's happening in the lung at the molecular level

in patients who are African American

as compared to patients who are Caucasian.

Do we need one therapy that's a one-size-fits-all

that will positively impact the outcome of all patients,

regardless of how different they are,

whether they have mild disease or more severe disease,

or do we need to consider the form of the disease,

and the severity of the disease, and its rate of progression,

and ensure that ultimately therapies are developed

specifically for each subset of patients.

So it's important to understand why some individuals

are more prone to having more severe disease than others.

So you talked a little bit about

treatment being a piece of the work that you're doing,

but I would imagine that primary prevention

is really also a big key,

because this is, scleroderma, for instance,

is something that someone can get down the road,

or could end up having it down the road.

So what does primary prevention look like

in the case of scleroderma or fibrosis,

and how are you looking into that as well?

That's an excellent question.

We know that there are likely to be

acquired changes or environmental triggers

that cause scleroderma,

at least in some people.

We don't really know what all those triggers are.

A few have been identified,

but those same triggers don't cause scleroderma

in everyone exposed to them,

so there's something that makes some people

more susceptible than others.

So for me, prevention is figuring out

who are the individuals who are more susceptible

to developing scleroderma.

What are the triggers that cause scleroderma?

Then prevention comes with knowing

individuals who are susceptible,

can avoid those triggers,

or once a therapy is developed,

it is used very early on in those who are susceptible

with very early signs

before the disease has a chance to set in

and cause what we call end stage fibrosis,

which currently is not reversible

and causes loss of organ function.

Fibrosis of the lung in scleroderma

is currently the leading cause of death in patients

because there is no treatment to reverse the fibrosis,

and the only option is to get a lung transplantation,

but there aren't enough donor lungs

and exact matches to go around,

and as a result, people die.

So if we can identify those people much earlier,

know they are likely to get to that stage,

and know how we can prevent it,

then we've prevented the burden of the illness,

the psychological burden, the physical burden,

the economic burden, we've prevented all of it,

which would be the ideal place to be.

What are some of the examples of environmental factors?

The environmental factors that have been reported

are somewhat different for different organs.

I can give you examples.

In the liver, we know hepatitis C,

a viral infection, can ultimately lead to

liver fibrosis, liver cirrhosis.

In the lung, we know historically

that coal miners who were exposed to silica dust

developed a form of lung fibrosis,

so that's an environmental factor.

But we're also constantly learning about

new triggers that we were not aware of,

and the last two years have been a great example of that

because there's data now suggesting that

individuals who were very ill, critically ill,

with COVID-19 and recovered

have now evidence of lung fibrosis.

So there's another viral etiology

linked to ultimately the development

of lung fibrosis.

So speaking of your research, you are a pioneer

because you created

a way of doing your investigations

in an organ culture system which was ex vivo.

So for our non-researcher listeners,

that means that it takes place outside of an organism,

so it's not in an animal or it's not in a human.

Tell us about that and how that came about,

because I just think it's so fascinating

and so incredible that you came up with this system

that's now being used and referenced

by other people in the field as well, right?

Right.

I want to say about 20 years ago,

we were doing research

focusing on genes that trigger fibrosis.

The models that we have available

for at least scleroderma and IPF are not good, the mouse models.

We don't have a model that truly recapitulates

what you see in the human disease.

We haven't been able to find that model.

Also, I've always had an interest

in developing therapies.

It is known that most of the molecules

that are very effective at curing diseases in mice

fail in human trials

because humans are different than mice.

So I was interested in knowing that the research that I do

ultimately is going to be applicable to the human disease,

but also that molecules that we may test

that may be antifibrotic, potential future therapies,

are likely to work in humans,

not just in mice.

So at the time I had a colleague who was getting human skin

that was discarded from plastic surgery

and using it for her immunology research,

so it was a different kind of research.

So I asked her if I could have some to try.

My interest was,

if I take human skin as an organ,

put it in a dish in the lab,

and give it the nutrients that it needs,

and put it at body temperature,

and if I introduced the genes we identified

as genes that can trigger fibrosis or the proteins,

can I cause fibrosis in this human skin?

Human skin is easy in a way to study for us

because you can measure fibrosis

by the extent of thickness of the skin,

because as the skin gets thicker and more fibrotic,

you can measure that thickness, literally.

-Mhm. -So I tried that and it worked.

The protein we initially introduced into the human skin

caused a beautiful fibrotic phenotype.

So as a result, we optimized the model,

working with what are the optimal timepoints,

what are the optimal concentrations,

how long can we keep the skin relatively healthy

in the setting of the lab?

Things along those lines.

Since then, we've used this model

in multiple publications and multiple projects

mostly to show that our research is relevant

and applicable to human tissues,

and thus ultimately the human disease.

So in a way it derisks a little bit

the therapies that you're developing

because you know they work in the human tissue

and not just in mice and not just in cells

cultured on plastic in the lab.

Right, which is really incredible

that you've found that model,

because I would imagine there are lots

of biomedical research questions

that we wish could be answered

straight into a human model,

or preferably a human model outside of a human

to get exactly to what you're talking about,

to speed up the process of investigation.

Exactly, and there's a lot of interest now

in what we call the organoids,

where various researchers, various labs,

are isolating separately the different cell types

in an organ or a tissue, such as the skin,

so maybe isolating the keratinocytes,

isolating the fibroblasts.

We studied different areas of the skin.

But then taking those cells and mixing them together

in a dish with maybe some collagen around

to give them something to stick to,

and calling that an organoid

to test in a human,

somewhat in a human model.

But for me, the skin was already assembled.

It's beautiful as it is.

It has all the components that you would imagine

you would have in any human, right?

So it seemed like the more appropriate way to go,

and simpler technically as well.

It's worked,

and the skin is one of the organ systems

that you would study in the diseases that you study,

so it makes total sense that

that's where you would land with that,

so I love that.

So what do you find most exciting

about your research?

What's your favorite aspect of it,

or maybe even a favorite story

of your research over the years?

The fact that no two days are alike

and that some of the most exciting discoveries

are accidental.

So for example, our lab has been developing this peptide,

which is a short stretch of amino acids

or a part of a protein,

as a treatment for fibrosis.

But when we discovered it

it was a completely accidental discovery.

We were actually working on these factors we identified

that cause fibrosis,

and we were trying to figure out how they did it.

So if you add a protein that causes fibrosis,

what are things after that step

downstream of it, that are changing?

What genes is it turning on, what genes is it turning off?

Are those genes, when it turns it on,

the way that it causes fibrosis, right,

the mechanism, or what mediates that process?

While we were doing that, we stumbled on this peptide

that at the beginning we thought that's what it was doing.

It was mediating the profibrotic response

of a factor we identified as a fibrotic factor.

We took it and we went to test it on its own

to see, if you added on its own

to cells or human skin in the organ culture we do,

will that peptide also cause fibrosis?

To our surprise, it had the total opposite effect.

So for me what's exciting in research

is having that prepared mind.

Like Louis Pasteur said,

"Chance only favors the prepared mind."

It's having that prepared mind

because some of the best discoveries in science,

in general, not just medical research,

but science in general, happen accidentally.

Yeah, I love accidental discovery.

We've talked about that a little bit

so far on Science Never Sleeps,

and I think that's really one of the big takeaways

for our audience from researchers,

is that discovery is never planned.

right, it happens just through the diligent work

of researchers who are asking a question,

or having a hypothesis, or having a thought

about what they think, and then running that down

and seeing, "Where does it go?"

Sometimes it can land in somewhere

that you completely didn't expect.

Exactly,

and the fun part of research, too, is,

I see research like a puzzle,

and every time we generate new pieces of data

you're adding a piece to the puzzle

to be able to get a clear picture

of what is happening.

So having the new data all the time,

and looking at it,

and thinking, "What does it mean?

How could we take it to the next step

and the next level?"

So there's a lot of problem solving

in research as well, which makes it more interesting

and more enjoyable, obviously.

So I think that's a really great segue

to my next question, which is about

connecting basic research to clinical work.

I feel like the work you're doing

is a really great example of that.

Can you speak to the importance of that connection

and sort of how you feel about what that process looks like?

Basic research always impacts clinical work,

because the discoveries you make at the bench

ultimately lead to identifying factors

that trigger or cause an illness

that can then be targeted

to impact the clinical outcomes.

It can lead to the discoveries like in our case

of this peptide that's antifibrotic,

so potential therapies that could be developed

to change how you take care of patients

with that particular disease.

So I feel like basic research

and clinical work are impacted by each other.

You can start with the clinical observations,

that this disease occurs

and there's not much out there in the literature

about why it occurs, and then decide

to take it to the bench and try and understand

what's happening in it.

You can start from the bench side,

where you make an observation that ultimately

may change how you treat patients,

or it may change

how you stratify patients for clinical trials,

knowing that patients with this particular protein

in their blood are going to respond better than others.

So they can be treated with this drug,

but then the other group that doesn't respond as well

needs another drug developed that would be more effective.

So in a way it's a marriage, right?

You cooperate, you help each other.

Leads in the clinical realm

are insights for the basic research,

and leads generated in basic research

can inform clinical work.

Now that you've discovered this peptide,

this part of a protein that you talked about,

what is the journey of that discovery now?

What happens next?

I didn't realize when I first came across the peptide

what is involved in developing any product

to get to the humans at the end,

but there's quite a bit involved.

So we've done a lot of the preclinical testing.

So you want to test to look for efficacy.

You want to test in different models,

under different conditions.

Then once you do that, there's a lot more

that has to be done, that's why drug development

takes so long.

Just examples of what needs to be done,

you got to check stability of the molecule.

How stable is it under different conditions,

different temperatures?

What is it soluble in?

If you're going to administer it to patients,

is it going to be in capsules?

Is it going to be in tablets?

Is it going to be injected?

Is it going to be oral?

You got to consider that.

You got to consider potential toxicity,

so you have to do all of the earlier toxicity studies,

looking as you increase the doses of it,

let's say, in mice,

do you see any evidence of toxicity

through blood work, through looking at the organs?

Different aspects of it.

So there's quite a bit that needs to be done

before you can even consider going to the FDA for approval

to start a safety trial, phase one trial, in humans.

All that testing takes time, and for a good reason,

because when you get to the humans

you want to know that the molecule that you have,

the drug you're going to administer,

is going to be safe, that you're not

going to cause harm, you're not going to cause people

to have horrible side effects.

So it's critical testing that really should be done,

and I appreciate why it needs to be done,

but it does take time

and it does take quite a bit of money as well.

So as far as the testing side of it,

is that where you continue to look for the research dollars

to support the testing because your team

is also investigating that side of it as well?

We're doing some of that,

so we're investigating some of the aspects

of all the testing that's required.

But a lot of it is beyond the funding

that an academic lab can have,

and that's why it's essential to partner with industry

who would have the resources to do all the necessary testing

and take it to the next level,

because it's the type of funding that's difficult to get

through grants, and it's actually substantial.

So it's very important to have that partnership at the end.

I think that's a great segue to talk about your work

with the National Scleroderma Foundation,

because that's a mechanism that can really

bring attention to this issue,

and I would imagine also connect funding

to places where it can make the most difference

where maybe there are those funding gaps.

Can you talk a little bit about your work

with the foundation

and sort of what you guys are trying to accomplish there?

Right.

The National Scleroderma Foundation

is a unique organization

because its mission involves

support for the patients, and their families,

and their caregivers.

It involves education about the disease,

increasing awareness about the disease,

advocacy to ensure there's enough funding

at NIH and other places to fund research on the disease,

but it also includes funding research directly.

So the National Scleroderma Foundation

does have research grants,

and I got involved many years ago

because I wanted to make an impact

more than what I could do in doing research at the bench.

I wanted to engage with the patients

and I wanted to be able to communicate with the patients,

to give them hope that there is research happening

on scleroderma, that we are making discoveries,

we are making progress, we are moving forward.

So I got involved for that reason.

So I'm currently the Vice Chair of the Board of Directors

of the National Scleroderma Foundation,

and I also oversee the research program.

Just over the past year, the Scleroderma Foundation

used award grants in the amount of about

a million dollars a year,

and just over the past year, we've been able to increase it

to $2.7 million a year,

which makes a huge difference for investigators,

especially the junior investigators

who are early in their career stage,

who need just to get started, something to give them the boost

to generate the early data that they need

to write the bigger grants to places like the NIH.

So I think the National Scleroderma Foundation

has actually been critical in launching the careers

of most of the individuals that we now consider experts

in the scleroderma field and senior leaders

in the scleroderma field.

They started with that launch of their career

with their first National Scleroderma Foundation grant.

You really have a soft spot for junior investigators

and for mentoring.

I do, that is definitely a soft spot.

It's one of my passions, one of my passions.

My career path was not easy.

I succeeded, I hope.

I continue to work towards success,

but I always think, "What have I learned

along the way and how can I pass it along

to those earlier in their career stages

to save them the time from the mistakes that I made

that could save them time?"

From the tips that I picked up along the way,

I could share that and they could learn it earlier,

benefit from it earlier.

So I've always had this passion

for supporting the careers of junior investigators.

Because of that, I've been very focused,

through the National Scleroderma Foundation,

on providing funding

for what we call early investigators

or new investigators, but also launched a year ago

a predoctoral award for graduate students

who are doing research on scleroderma

just to start supporting them and encouraging them

at an even earlier stage of their career

because it's important to nurture this next generation.

We need the pipeline of researchers.

We don't have enough researchers in the U.S.

We have fewer people engaged in academic research

because it's hard.

You have to struggle, you have to get grants.

A lot of grants get rejected, manuscripts get rejected.

Ultimately, perseverance helps you succeed,

but we need to encourage more junior investigators

to get into the field and show them

how exciting it can be

and how much fun, really, research is,

but also give them the support and the little push

that they need to help them succeed

and to just boost a little bit their career,

to help them get there so they can see

that there is a path forward for them.

Dr. Feghali-Bostwick, thank you so much

for joining us on Science Never Sleeps.

Thank you for having me.

We've been talking to Dr. Carol Feghali-Bostwick

about fibrosis and her research

and the future of treatment for patients.

You can find out more about the research happening at MUSC

by visiting Research.MUSC.edu.

Have an idea for a future episode?

Send us an email at ScienceNeverSleeps@MUSC.edu.

Science Never Sleeps is produced by the Office

of the Vice President for Research

at the Medical University of South Carolina.

Special thanks to Caren Doueiry

in the MUSC College of Graduate Studies

Science Writing program for scripting support,

as well as the Office of Instructional Technology

and Faculty Resources for production support

on this episode.

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