Foundation Celebrates 2026 Scleroderma Research Grant Awardees

The National Scleroderma Foundation is proud to announce the 2026 Scleroderma Research Grant Award recipients.

To date, the National Scleroderma Foundation has proudly awarded more than $35 million in scleroderma research grants. These projects received the peer‑review committee’s highest ranking for scientific design quality and the prospect of advancing the scleroderma body of knowledge.

Because grants are spread over two or three years, in any given year, the Foundation has funding commitments to more than two dozen ongoing projects. Our commitment to these projects is a driving force behind fundraising efforts such as Stepping Out to Cure Scleroderma walks.

Click on the photos below to learn more about the research grant recipient and their research project.

2026 Grant Award Recipients

Gulsen Ozen, MD

Indu Sapra, MD Memorial Research Grant recipient

Mapping Systemic Sclerosis in the US: Geographic Patterns in Prevalence, Complications, Cancer Links, and Healthcare Utilization
University of Iowa Health Care
New Investigator Award

Systemic sclerosis (SSc) is the deadliest autoimmune disease. It causes severe disability and the lowest quality of life among ~200 chronic diseases. The US has the highest rates of SSc and related deaths worldwide, yet little is known about how the disease and its complications (lung scarring and high pressure in the lung arteries) vary across the country. Genetics play a smaller role in SSc than other autoimmune diseases. This means that environment, sociodemographics, and access to healthcare may strongly influence who develops SSc and how severe it becomes. In some patients, SSc develops around the time of cancer, raising the possibility that cancer may trigger or worsen the disease.

This project will use Komodo data, analyzed at the 3-digit ZIP code level, to uncover patterns in SSc occurrence, organ complications, cancer co-occurrence and timing, and healthcare use across the US. A follow-up study will relate these findings to survival.

By mapping these patterns, we aim to understand how geography, healthcare and other non-genetic factors like cancer shape the risk and severity of SSc. These insights will help guide targeted strategies for screening (organ problems or cancer), prevention, and care, ultimately reduce disparities, and help patients live longer, healthier lives.

Daniel Batlle, MD

Mark Flapan Award recipient

A novel ACE2 protein for Scleroderma Kidney
Northwestern University
Established Investigator Award

Scleroderma kidney is a rare but very severe complication of systemic sclerosis or scleroderma, where there is a severe blood pressure increase with deterioration of kidney function, to the point that the kidneys fail and require dialysis. Currently used medications called ACE inhibitors are sometimes very effective but, overall, they have not been able to change the course of the disease for most patients, and the mortality remains very high. In addition, these drugs are not recommended for use in scleroderma patients who have not yet developed a kidney crisis because when used preventatively the outcomes were worse than when not used. Therefore, there is an urgent need to identify novel treatments to improve outcomes in patients with scleroderma kidney. To be able to develop therapies for humans, it is necessary to first try them in animal models that mimic human kidney complications in patients, and currently, there are no good models for this purpose. In this proposal, we will use an existing mouse model where we have found that many of the kidney features of patients with Scleroderma Kidney can be found and therefore studied in great detail. Using this mouse model, we will determine the benefit of giving a novel soluble ACE2 protein to these mice for several weeks. The effectiveness of this protein injected into mice will be compared with the effectiveness of currently used ACE inhibitors. We anticipate that our study will provide strong evidence that our novel therapy in an appropriate animal model of scleroderma kidney will lay a strong foundation for moving this new drug to the clinic.

Matthew Dapas, PhD

Walter and Marie Coyle Award recipient

Evaluating a role for polysialic acid as a diagnostic, prognostic and therapeutic target in systemic sclerosis
Northwestern University Feinberg School of Medicine
New Investigator Award

An effective immune system relies on its ability to distinguish between healthy cells and those that are compromised or foreign, allowing it to respond precisely to threats while minimizing damage to the body’s own tissues. Human leukocyte antigen (HLA) proteins are crucial in this process, as they bind to and present foreign proteins to immune cells, facilitating immune recognition. Consequently, HLA genes are consistently identified as the strongest genetic risk factors for autoimmune diseases, where the immune system mistakenly targets the body’s own cells. Different versions of HLA proteins are also associated with different subtypes of these diseases.

Systemic sclerosis, or scleroderma, is a serious autoimmune disease that causes the skin and internal organs to become thick and stiff. In scleroderma, certain HLA genes are linked to specific types of the disease and its severity. This project aims to use genetic sequencing and single-cell gene expression analysis to study these

HLA genes in people with different types of scleroderma. The goal is to identify HLA-mediated pathways that contribute to clinical variability among patients. A deeper understanding of these mechanisms may lead to the development of more personalized and effective treatments for scleroderma patients.

Eliza Tsou, PhD

Marta Marx Fund for the Eradication of Scleroderma recipient

Endothelial Senescence and the cGAS-STING Pathway: Drivers of Vasculopathy in SSc
University of Michigan
Established Investigator Award

Systemic sclerosis (SSc), or scleroderma, is a rare, serious autoimmune disease that causes blood vessel damage and widespread tissue scarring. People with SSc suffer from reduced blood flow to their skin and organs, but the reasons for this blood vessel injury are not well understood. Recent research suggests that blood vessel cells in SSc become “senescent”, a state where the cells stop working properly and release harmful substances that lead to inflammation and more tissue damage. Our research focuses on a process where damaged cell parts, called mitochondrial DNA, accumulate outside the nucleus of blood vessel cells.

This triggers a pathway known as cGAS-STING, which may drive the harmful cell changes and inflammation seen in SSc. We also suspect that bits of mitochondrial DNA and immune proteins found in the blood might be clues, or markers, of blood vessel injury. This project will investigate exactly how mitochondrial DNA and the cGAS-STING pathway lead to blood vessel damage in SSc, and explore whether measurement of these molecules in patient blood relate to visible blood vessel problems. Our findings could point toward new ways to diagnose and eventually treat blood vessel damage in SSc.

Rachel Knipe, MD

Debra Lurvey Memorial Award recipient

Targeting Vascular Permeability through Inhibiting Endothelial 2a. NEW INVESTIGATOR GRANT ROCK2 in SSc ILD
Massachusetts General Hospital
Established Investigator Award

Systemic Sclerosis (SSc) is an autoimmune disease with tissue fibrosis, or scarring, that can affect many organs. Lung fibrosis, also known as SSc associated interstitial lung disease (SSc-ILD), is the leading cause of death in SSc. There is a great need for therapies to stop the development and progression of SSc-ILD.

Endothelial cell (EC) injury and vasculopathy precede fibrosis as an early event in disease pathogenesis. EC sense injury through exposure to circulating factors and changes in their environment like stiffness. Rho kinase (ROCK), a mechanosensor, regulates EC barrier function. We propose that in SSc-ILD, EC injury increases permeability and tissue stiffness, causing persistent EC dysfunction and fibroblast activation that promote fibrosis. Restoring pulmonary vascular integrity via inhibition of EC ROCK in SSc could have great therapeutic value.

Our preliminary data show that lung EC in SSc-ILD have increased ROCK activity, and that EC-specific ROCK2 deletion is protective in a model of lung fibrosis. We hypothesize that therapeutic EC ROCK2 inhibition will prevent SSc-ILD. We will use endothelial ROCK2 deletion mice in a pump systemic bleomycin model to determine how ROCK2 drives SSc-ILD (Aim 1) and how EC ROCK2 dependent mechanotransduction promotes endothelial dysfunction associated with SSc-ILD (Aim 2).

Kaveh Ardalan, MD, MS

Engaging Juvenile Localized Scleroderma Patients and Caregivers to Inform Mental Health Intervention Development
Duke University
Established Investigator Award

At half of doctor’s visits, patients with juvenile localized scleroderma (JLS) report negative effects on their quality of life. Living with JLS can be stressful due to the damaging effects of JLS on skin and underlying tissues, which can be disabling and disfiguring. Treatments for JLS often cause side effects are stressful to cope with. In many other pediatric rheumatic diseases, depression and anxiety are common due to disease and treatment related stressors. But there are no published studies defining how often JLS patients experience depression and anxiety, who is at highest risk, how depression and anxiety influence JLS patients’ medication adherence, or how to support of JLS patients’ mental health. This study will define the scope of mental health impact in JLS and lay groundwork for future mental health supports tailored to JLS patients’ unique experiences. We will use surveys to determine the mental health impact of JLS, risk factors for mental health challenges in JLS patients, and relationships of depression and anxiety to medication nonadherence. We will also engage JLS patients and caregivers in focus group interviews to gather perspectives on the design of mental health interventions to support JLS patients.

Samuel Good, MD

Development of a Novel Patient Reported Outcome Measure for Patients with Systemic Sclerosis-Associated Gastrointestinal Disease
The Regents of the University of California, Los Angeles
New Investigator Award

Currently, there are no therapies available that stop the progression of systemic sclerosis in the gastrointestinal (GI) tract. Symptoms of the GI tract include difficulty swallowing, heartburn, nausea, vomiting, diarrhea, constipation and abdominal pain, amongst others. These are symptoms that people living with scleroderma describe as particularly bothersome. They contribute to disability and risk of death for those living with the disease. One major reason for why we cannot stop the progression of scleroderma in the GI tract is that there are no tools that accurately measure disease progress and response to treatments in the GI tract. Without a way to measure how therapies affect GI disease in scleroderma, it is impossible for clinical trials to evaluate new drugs that could potentially treat these symptoms. The purpose of this study is to develop a tool, called a patient reported outcome measure, that accurately measures patient symptoms and can be used in clinical trials. This tool will allow for researchers to conduct trials specifically for drugs that target the progression of scleroderma GI disease. This has the potential to reduce symptom burden and improve outcomes for people living with scleroderma GI disease.