Monique Evangeline Hinchcliff
· Director of Clinical and Translational ResearchVerifiedYale University · Rheumatology
Active 2007–2026
About
Dr. Monique Evangeline Hinchcliff is an Associate Professor of Medicine specializing in Rheumatology, Allergy & Immunology at Yale School of Medicine. She serves as the Director of the Yale Scleroderma Program and the Director of Clinical and Translational Research in the Internal Medicine Rheumatology section. Additionally, she is the Associate Director of the Clinical and Translational Research Accelerator at Yale. Dr. Hinchcliff earned her medical degree from Rosalind Franklin University Chicago Medical School and completed her residency in medicine at Norwalk Hospital in Connecticut. She pursued rheumatology fellowship training at Northwestern University Feinberg School of Medicine in Chicago, where she also obtained a Master of Science degree in Clinical Investigation. Her research program focuses on clinical, interventional, and observational studies aimed at better understanding systemic sclerosis and identifying new and repurposed treatments for patients with this condition. Dr. Hinchcliff maintains active research collaborations both within the United States and internationally. Clinically, she leads a multidisciplinary team of specialists dedicated to the care of patients with systemic sclerosis. She is actively involved in ongoing clinical trials to provide patients access to the latest potentially beneficial treatments.
Research topics
- Medicine
- Internal medicine
- Physical therapy
- Pathology
- Intensive care medicine
- Psychiatry
- Immunology
- Clinical psychology
- Emergency medicine
- Psychotherapist
- Psychology
- Cancer research
- Biology
- Demography
Selected publications
Best Practice & Research Clinical Rheumatology · 2026-04-01
articleCorrespondingLara D. Veeken · 2026-04-20
articleOBJECTIVES: Cardiovascular death is the second leading cause in systemic sclerosis (SSc), with coronary microvascular dysfunction (CMVD) playing a key role. PET-derived myocardial blood flow (MBF) and flow reserve (MFR) offer a validated, non-invasive way to assess CMVD. We studied the prevalence of impaired MFR in SSc and its association with vasodilator or immunomodulatory therapy. METHODS: SSc patients who underwent dynamic 82-Rubidium PET myocardial perfusion imaging (MPI) at Yale New Haven Hospital (July 2016 to April 2025) were studied. Patients were matched 3:1 with controls without autoimmune rheumatologic disease based on age, sex, BMI and cardiovascular comorbidities. Abnormal MFR was defined as <2.0. RESULTS: The cohort included 67 SSc patients (87% female, age: 61 ± 11 years, 21% diffuse cutaneous SSc, SSc duration: 12 ± 10 years) and 201 controls. Rest MBF was higher in SSc (1.14 [IQR 0.91-1.39] ml/g/min) vs controls (1.00 [IQR 0.78-1.25]; P = 0.01), while MFR was lower (2.17 [IQR 1.84-2.57] vs 2.44 [IQR 1.96-2.96]; P = 0.01). Stress MBF was similar (2.47 [IQR 1.99-2.82] vs 2.43 [IQR 1.91-3.04]; P = 0.85). Multivariable analysis showed MMF use linked to lower odds of abnormal MFR (OR 0.09 [95% CI 0.01-0.56]; P = 0.017), while calcium channel blockers (OR 7.77 [1.93-42.53]; P = 0.008) and statins (OR 7.14 [1.86-36.87]; P = 0.008) increased odds. CONCLUSIONS: PET MPI reveals reduced MFR in SSc. Treatment associations, including MMF, should be interpreted cautiously given the retrospective design. PET-derived MFR may serve as a non-invasive marker of vascular involvement, warranting prospective validation.
ACG Case Reports Journal · 2025-04-01 · 1 citations
articleOpen accessWe present a case of a 49-year-old woman with diffuse cutaneous systemic sclerosis with refractory gastroesophageal reflux disease and dysphagia for pills and solid foods. Esophagogastroduodenoscopy revealed gastroesophageal intussusception. Despite several interventions including esophageal stent placement, dysphagia persisted. Owing to refractory severe symptoms, the patient underwent a laparoscopic hiatal hernia repair combined with endoscopic transoral incisionless fundoplication. The patient tolerated the intervention well and dysphagia resolved. Although an obscure persistent dysphagia in SSc patients, gastroesophageal intussusception should be considered. This case underscores the need for persistence in the diagnostic evaluation of gastrointestinal symptoms in patients with SSc and highlights the need for a multidisciplinary team care approach.
The Lancet Rheumatology · 2025-04-02 · 12 citations
article1st authorCorrespondingCurrent Opinion in Rheumatology · 2025-08-20
articleOpen accessCorrespondingPURPOSE OF REVIEW: Patients with systemic sclerosis (SSc) often seek advice regarding diet including functional foods, and complementary and alternative medicine (CAM) as adjunctive therapies. This review summarizes existing literature regarding these approaches. RECENT FINDINGS: Study results of low Fermentable Oligosaccharides, Disaccharides, Monosaccharides, And Polyols (FODMAP), Mediterranean and ketogenic diets suggest symptom reduction and beneficial microbiota modulation in SSc, though sample sizes are small. Nitrate-rich and antioxidant supplements such as omega-3 fatty acids show promise in lowering inflammation and oxidative stress in the circulation. Herbal remedies like curcumin have demonstrated antifibrotic properties in preclinical models. Topical agents (e.g., rosemary oil, vitamin E gel) and nutritional vitamins (e.g., C, D, E) are also frequently used, though robust clinical trials are lacking. SUMMARY: CAM, dietary interventions, and functional foods may aid in SSc management, but more rigorous research is needed to provide definitive evidence.
European Respiratory Journal · 2025-05-15 · 5 citations
articleOpen accessObjective The lungs of patients with systemic sclerosis-associated interstitial lung disease (SSc-ILD) contain inflammatory myofibroblasts that arise in association with fibrotic stimuli and perturbed innate immunity. The cytosolic DNA-binding receptor cyclic GMP-AMP synthase (cGAS) is implicated in inflammation and fibrosis, but its involvement in SSc-ILD remains unknown. We examined cGAS expression, activity and therapeutic potential in SSc-ILD using human biospecimens, cultured fibroblasts, precision-cut lung slices and a well-accepted animal model. Methods Expression and localisation of cGAS, cytokines and type 1 interferons were evaluated in SSc‑ILD lung tissues, bronchoalveolar lavage fluid and isolated lung fibroblasts. CGAS activation was assessed in a publicly available SSc-ILD single-cell RNA-sequencing dataset. Production of cytokines, type 1 interferons and α-smooth muscle actin elicited by transforming growth factor-β1 or local substrate stiffness was measured in normal human lung fibroblasts via quantitative reverse transcription PCR, ELISA and immunofluorescence. Small molecule cGAS inhibition was tested in cultured fibroblasts, human precision-cut lung slices and the bleomycin pulmonary fibrosis model. Results SSc-ILD lung tissue and bronchoalveolar lavage fluid were enriched for cGAS, cytokines and type 1 interferons. The cGAS pathway showed constitutive activation in SSc-ILD fibroblasts and was inducible in normal human lung fibroblasts by transforming growth factor-β1 or mechanical stimuli. In these settings, and in precision-cut lung slices, cGAS expression was paralleled by the production of cytokines, type 1 interferons and α-smooth muscle actin, which was mitigated by a small molecule cGAS inhibitor. These findings were recapitulated in the bleomycin mouse model. Conclusion cGAS signalling contributes to pathogenic inflammatory myofibroblast phenotypes in SSc‑ILD. Inhibiting cGAS or its downstream effectors represents a novel therapeutic approach.
Trials · 2025-11-12 · 1 citations
articleOpen accessBACKGROUND: Researchers are mandated ethically to share study results with participants, and funding agencies emphasize dissemination to others with relevant lived experience. Many researchers, however, find it difficult to communicate study purposes, methods, results, and significance to patients. Our Scleroderma Patient-centered Intervention Network (SPIN) piloted "co-presentation," which involves researchers and patient partners jointly presenting results to other patients. The SPIN Patients Alongside Investigators in Research-Sharing (SPIN-PAIRS) Trial will be conducted as part of a 90-min virtual research event for people with systemic sclerosis (SSc, scleroderma) and will compare patient and researcher partner co-presentation versus researcher-alone presentation. Primary outcomes will be event attendee ratings of presentations on (1) information completeness, (2) understandability, (3) relevance to patients, and (4) trust in findings. Secondary objectives are to (1) conduct subgroup analyses of primary outcomes by participant characteristics (gender, age, race or ethnicity, country, education level, health literacy) and (2) use qualitative interviews to better understand outcome ratings and inform co-presentation. METHODS: This will be a mixed-method study with (1) a two-arm parallel superiority randomized controlled trial embedded in a patient-oriented research event and (2) interviews with patient and researcher co-presenters, separately, and with trial participants. Pre-event, researchers will be selected to present via an open call for abstracts and a patient-led selection committee. To avoid presentation-related biases, pre-event, researchers will record researcher-alone presentations. They will then receive co-presentation training and develop co-presentations with patient partners, which will also be recorded. Eligible trial participants will be adults aged 18 or older who indicate they have been diagnosed with SSc by a physician. We will recruit participants via social media and email lists from our multinational SPIN Cohort and from patient organization partners to attend the event and rate presentations. Participants will be recruited to register for the event beginning in August 2025. Registered participants will be invited to confirm their registration and enroll in the trial on the day of the event. We will require at least 116 participants for ≥ 80% power but will not restrict the number of enrollees. We will randomly assign event attendees 1:1 to virtual rooms with (1) four pre-recorded patient-researcher co-presentations or (2) four pre-recorded researcher-alone presentations. The same studies will be presented in each arm with live questions and answers after each presentation in each virtual room. Attendees will rate each presentation immediately following the presentation. Participants will not be informed that they are part of a randomized trial, or that two conditions are being compared and will be blind to study comparisons and hypotheses. Presenters will not be blinded during the event. We will compare outcomes, all measured via 0-10 numerical rating scales, using linear mixed models with four observations per participant for each outcome (one observation for each presentation). Interviews will be conducted < 2 weeks post-event, and verbatim transcripts will be analyzed using an inductive-deductive thematic approach. DISCUSSION: Findings will contribute to the evidence base on effective strategies for sharing results with study participants and others with relevant lived experience. Trial registration ISRCTN12805381 ( https://www.isrctn.com/ISRCTN12805381 ).
Imaging-Based Mortality Prediction in Patients with Systemic Sclerosis
Lecture notes in computer science · 2025-11-13
book-chapterOpen accessJACC Case Reports · 2025-02-01
articleOpen accessSenior authorCorrespondingBACKGROUND: Systemic sclerosis (SSc) cardiomyopathy has a prevalence of 7 to 39% and is associated with increased mortality. Despite this, little evidence informs SSc cardiomyopathy treatment. CASE SUMMARY: We present a patient with diffuse cutaneous SSc with acute heart failure. Extensive workup supported a diagnosis of SSc myopericarditis, although endomyocardial biopsies were unrevealing. She received intravenous cyclophosphamide and glucocorticoids and achieved significant and prolonged recovery. DISCUSSION: Our patient presented with systolic dysfunction as opposed to diastolic dysfunction that is more typical in patients with SSc-cardiomyopathy. Endomyocardial biopsies lacked T-lymphocyte infiltration that may be due to sampling error because >17 samples are needed to diagnose myocarditis in >80% of cases.
Gastrointestinal manifestations of systemic sclerosis: current approaches and emerging therapies
Current Opinion in Rheumatology · 2025-07-11 · 10 citations
articleOpen accessPURPOSE OF REVIEW: This review highlights recent advances in the understanding and management of gastrointestinal manifestations in systemic sclerosis (SSc). It is intended for clinicians and researchers aiming to improve diagnostic accuracy and therapeutic strategies in managing SSc-related gastrointestinal disease. RECENT FINDINGS: Gastrointestinal involvement in SSc is highly variable in terms of clinical presentation, symptom severity, progression, timing of onset, and response to treatment. Emerging research highlights early immune-mediated damage to neural and muscular gastrointestinal tissues, microbiome alterations, and vascular dysfunction - particularly in patients with late-onset gastrointestinal disease - as key factors guiding the development of personalized, precision-based approaches for well defined patient subgroups. Recent studies underscore the value of early, objective assessment of gastrointestinal motility using tools like whole-gut transit scintigraphy and abdominal vascular ultrasound. New treatment strategies are also being explored for severe manifestations, including investigating mechanisms behind acid-suppressive therapy-resistant gastroesophageal reflux disease and implementing adjunctive therapies for gastrointestinal dysmotility. SUMMARY: Gastrointestinal involvement in SSc poses a complex clinical challenge, particularly in patients with severe dysmotility and symptoms refractory to standard management strategies. This review offers timely, evidence-based insights to support clinicians in delivering more personalized and effective patient care and highlights critical gaps to address in future research.
Recent grants
NIH · $400k · 2018
Pathogenic Wnt-beta catenin target genes in macrophages and fibrosis
NIH · $2.6M · 2019–2025
NIH · $390k · 2016
Frequent coauthors
- 231 shared
John Varga
- 212 shared
Virginia Steen
Georgetown University Medical Center
- 205 shared
Maureen D. Mayes
The University of Texas Health Science Center at Houston
- 202 shared
Robyn T. Domsic
University of Pittsburgh
- 201 shared
Leland W.K. Chung
Stanford University
- 186 shared
Laura K. Hummers
Johns Hopkins University
- 186 shared
Vivien Hsu
Sir Charles Gairdner Hospital
- 178 shared
Daniel E. Fürst
University of Florence
Education
- 2000
M.D., Medicine
Yale School of Medicine
- 1995
M.S., Immunology
University of California, San Francisco
- 1991
B.S., Biology
University of California, San Francisco
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