About Us - The Scleroderma Research Foundation

Research is the key…

The Scleroderma Research Foundation (SRF) was established in 1987 by patient turned activist Sharon Monsky, when research on this potentially life threatening illness was nearly nonexistent. Since our founding, we’ve stood firm in our belief that the best way to help scleroderma patients is to fund the most promising medical research aimed at improved therapies and a cure. The SRF is America's largest nonprofit investor in scleroderma research. Patients and their loved ones find hope in the fact the SRF is dedicated exclusively to funding medical research that will help them live longer, fuller lives. Thanks in large part to the SRF and its many generous donors, research and awareness is progressing at a faster pace than ever before.

The SRF funds research investigators at some of the top universities in the United States and abroad, including Dartmouth, Harvard, Johns Hopkins, Royal Free and University College in the UK, Stanford University, Northwestern, Boston University, the University of Michigan, the University of Washington and others. Led by a Scientific Advisory Board comprised of some of the most highly-regarded scientists in the nation, the SRF's research program brings together experts from the fields of immunology and vascular biology as well as cutting-edge technology for the benefit of scleroderma patients.

The SRF is proud to maintain its position as the single largest nonprofit funding source for scleroderma research and devotes a greater percentage of its annual budget to scleroderma research, more than any other nonprofit organization.

Medical research to find better treatments for scleroderma patients is both time-consuming and expensive. Thanks entirely to thousands of supporters and generous donors, the SRF is able to expedite research progress and bring top scientists into the field of scleroderma research. The unique collaborative approach conceived by founder Sharon Monsky is enabling scientists from leading institutions across the nation—and around the world—to work together and develop an understanding of how the disease begins, how it progresses and what can be done to slow, halt or reverse the disease process.

Centers of Excellence

As another core feature of its research program, the SRF continues to provide funding to establish and support Scleroderma Centers where clinical research can be advanced. At these Centers, clinicians with large numbers of patients can collaborate with researchers and new scleroderma doctors and specialists can be trained.

Next Generation Investigators

Knowing that future discovery will come from the next generation of scientists, the SRF continues to provide grants to young investigators. Postdoctoral fellowship grants allow researchers to enter the field of scleroderma research and work alongside established investigators. As an indicator of success, several SRF-funded fellows are now dedicating their early careers to the field of scleroderma research.

Annual Scientific Workshop

Each year, the SRF hosts a Scientific Workshop where SRF-funded researchers and leaders from academia and industry engage in high level discussions about the state of scleroderma research. In addition, the SRF supports important educational initiatives such as the International Scleroderma Workshop. Collectively, these programs promote the sharing of ideas and new discoveries that further progress toward a cure.

Current IRS Form 990 and audited financial statements are available for review as Adobe PDF downloads in the Legal Notices and Privacy Information section of this website.

The continued success of the SRF research program is entirely dependent upon charitable gifts. These gifts come in many forms from generous people around the world who recognize that the SRF is dedicated to solving the mystery of scleroderma.

The SRF administrative offices are led by:

Amy Hewitt
Executive Director

Alex Gonzalez
Director of Development

Brendan Doherty
Director of Communications

 

 
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Research News

M10, a caspase cleavage product of the hepatocyte growth factor receptor, interacts with Smad2 and demonstrates antifibrotic properties in vitro and in vivo.

Author: Atanelishvili I, Shirai Y, Akter T, Buckner T, Noguchi A, Silver RM, Bogatkevich G
Date Published: April-2016
Source: Translational Research

Hepatocyte growth factor receptor, also known as cellular mesenchymal-epithelial transition factor (c-MET, MET), is an important antifibrotic molecule that protects various tissues, including lung, from injury and fibrosis. The intracellular cytoplasmic tail of MET contains a caspase-3 recognition motif "DEVD-T" that on cleavage by caspase-3 generates a 10-amino acid peptide, TRPASFWETS, designated as "M10". M10 contains at its N-terminus the uncharged amino acid proline (P) directly after a cationic amino acid arginine (R) which favors the transport of the peptide through membranes. M10, when added to cell culture medium, remains in the cytoplasm and nuclei of cells for up to 24 hours.

Esophageal dilatation and interstitial lung disease in systemic sclerosis: a cross-sectional study

Author: C. Richardson, R. Agrawal, J. Lee, O. Almagor, R. Nelson, J. Varga, M. Cuttica, J. D′Amico Dematte, R. Chang, M. Hinchcliff,
Date Published: February-2016
Source: Science Direct

A patulous esophagus on high-resolution computed tomography (HRCT) of the thorax is frequently observed in patients with systemic sclerosis (SSc). Microaspiration has been purported to play a role in the development and progression of SSc interstitial lung disease (ILD), but studies examining the role of microaspiration in SSc-ILD have yielded conflicting results. This study was conducted to determine the association between esophageal diameter and SSc-ILD.

Integrated long non-coding RNA analyses identify novel regulators of epithelial-mesenchymal transition in the mouse model of pulmonary fibrosis

Author: Hao Sun, Junjie Chen, Wenyi Qian, Jiang Kang, Jun Wang, Lei Jiang, Li Qiao, Wei Chen and Jinsong Zhang
Date Published: January-2016
Source: Journal of Cellular and Molecular Medicine

Idiopathic pulmonary fibrosis (IPF) is a chronic fatal lung disease characterized by aberrant accumulation of fibroblast population and deposition of extra cellular matrix. Increasing evidence support that epithelial-mesenchymal transition (EMT) of alveolar epithelial cells is a critical process in the pathogenesis of IPF. Although delivery of bleomycin to induce acute lung injury is the most well-studied animal model of pulmonary fibrosis, there is considerable interest to pursue other models to understand the common and/or specific pathological mechanisms. In this study, we established a mouse model of pulmonary injury and progressive interstitial fibrosis via intraperitoneal injection of paraquat, a widely used herbicide known to cause pulmonary fibrosis in human.

CD4+ Group 1 Innate Lymphoid Cells (ILC) Form a Functionally Distinct ILC Subset That Is Increased in Systemic Sclerosis

Author: Florence Roan, Thomas A. Stoklasek, Elizabeth Whalen, Jerry A. Molitor, Jeffrey A. Bluestone, Jane H. Buckner and Steven F. Ziegler
Date Published: January-2016
Source: The Journal of Immunology

Innate lymphoid cells (ILC) are a heterogeneous group of cellular subsets that produce large amounts of T cell–associated cytokines in response to innate stimulation in the absence of Ag. In this study, we define distinct patterns of surface marker and cytokine expression among the ILC subsets that may further delineate their migration and function. Most notably, we found that the subset previously defined as group 1 ILC (ILC1) contains CD4+ CD8−, CD4− CD8+, and CD4− CD8− populations.

Treprostinil iontophoresis improves digital blood flow during local cooling in systemic sclerosis

Author: Florence Gaillard-Bigot, Matthieu Roustit, Sophie Blaise, et al
Date Published: January-2016
Source: Microcirculation

Severe Raynaud's syndrome and digital ulcers are the most prevalent manifestations of systemic sclerosis (SSc) peripheral microvascular disease. We tested whether treprostinil iontophoresis on the finger pad of patients with SSc would improve digital blood flow during hand cooling.

News for Patients

Predictors of long-term outcomes in patients treated with riociguat for pulmonary arterial hypertension: data from the PATENT-2 open-label, randomised, long-term extension trial

Author: Patricia Inacio
Date Published: April-2016
Source: Scleroderma News

Researchers recently discovered a natural molecule, the M10 peptide, that can significantly decrease fibrosis in a mouse model of scleroderma. The study, “M10, a caspase cleavage product of the hepatocyte growth factor receptor, interacts with Smad2 and demonstrates antifibrotic properties in vitro and in vivo,” was published in the journal Translational Research. Systemic sclerosis, also known as scleroderma, is a chronic systemic autoimmune disease characterized by excessive deposition of collagen, leading to fibrosis in several organs, which can ultimately result in organ failure. Effective treatments targeting fibrosis in systemic sclerosis patients are lacking.

Predictors of long-term outcomes in patients treated with riociguat for pulmonary arterial hypertension: data from the PATENT-2 open-label, randomised, long-term extension trial

Author: H. Ghofrani, F. Grimminger, E. Grünig, Y. Huang, et al
Date Published: April-2016
Source: The Lancet

Pulmonary arterial hypertension is a chronic disease associated with poor long-term outcomes. Identifying predictors of long-term outcome in pulmonary arterial hypertension is important to assess disease severity and guide treatment. We investigate associations between efficacy parameters and long-term outcomes in patients with pulmonary arterial hypertension receiving riociguat in the PATENT-2 study. We also present safety and efficacy data from the final data cutoff of PATENT-2, where most patients had received at least 2 years of riociguat treatment.

Predictors of long-term outcomes in patients treated with riociguat for pulmonary arterial hypertension: data from the PATENT-2 open-label, randomised, long-term extension trial

Author: H. Ghofrani, F. Grimminger, E. Grünig, Y. Huang, et al
Date Published: April-2016
Source: The Lancet

Pulmonary arterial hypertension is a chronic disease associated with poor long-term outcomes. Identifying predictors of long-term outcome in pulmonary arterial hypertension is important to assess disease severity and guide treatment. We investigate associations between efficacy parameters and long-term outcomes in patients with pulmonary arterial hypertension receiving riociguat in the PATENT-2 study. We also present safety and efficacy data from the final data cutoff of PATENT-2, where most patients had received at least 2 years of riociguat treatment.

Prediction of improvement in skin fibrosis in diffuse cutaneous systemic sclerosis: a EUSTAR analysis

Author: Rucsandra Dobrota, Britta Maurer1, Nicole Graf, Suzana Jordan, Carina Mihai, Otylia Kowal-Bielecka, Yannick Allanore, Oliver Distler
Date Published: March-2016
Source: Annals of the Rheumatic Diseases

Improvement of skin fibrosis is part of the natural course of diffuse cutaneous systemic sclerosis (dcSSc). Recognising those patients most likely to improve could help tailoring clinical management and cohort enrichment for clinical trials. In this study, we aimed to identify predictors for improvement of skin fibrosis in patients with dcSSc.

Large Scleroderma Study Offers Genetic Map, Identifies Patients at Risk for Pulmonary Hypertension

Author: Margarida Azevdeo
Date Published: April-2016
Source: Scleroderma News Today

A research team with scientists from the University of Granada in Spain and the Spanish National Research Council (CSIC) has carried out the largest scleroderma study to date, creating a complete genetic map of the disease with the genetic analysis of more than 5,000 patients.

Ways to Give

There are many ways that you can support the work of the Scleroderma Research Foundation. We are grateful for your commitment to helping the SRF fund research that will result in improved therapies and, ultimately, a cure.

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