Hayek Lab University of Texas Medical Branch

What we do

Inflammation is the thread.

We start from a clinical problem, find the molecule that predicts it, work out why that molecule matters, and put the result back in front of the clinician. Two programs apply that approach where the risk is highest.

01

Inflammation and Cardiovascular-Kidney-Metabolic Disease

Heart, kidney, and metabolic disease tend to strike the same patients, and inflammation runs through all three. We study the immune signals that pass from one organ to another and turn them into biomarkers clinicians can act on.

The lab's best-known work is on suPAR, the soluble urokinase plasminogen activator receptor. Over a decade we established it as an independent predictor of new chronic kidney disease and traced its mechanism to a tripartite complex with APOL1 risk variants and αvβ3 integrin on podocytes. We then extended the findings to acute kidney injury and showed in mice that suPAR modulates monocyte function to promote atherosclerosis. We now describe suPAR as a compartmentalized signaling system in cardiovascular-kidney-metabolic syndrome: membrane uPAR drives local inflammation and remodeling, while soluble suPAR signals to distant organs, where persistent signaling contributes to disease.

Lines of work

  • suPAR and the kidney: new chronic kidney disease, declining filtration, acute kidney injury, and scarring of the kidney's filters (FSGS)
  • Mechanism: APOL1, αvβ3 integrin, monocyte priming, uPAR isoforms
  • Atherosclerosis, heart failure, and the cardiorenal axis
  • Inflammation and outcomes in COVID-19 and critical illness
  • Genetics of suPAR and multi-omics integration
Schematic of the kidney panel of a three-organ figure. At left, dysregulated innate immunity produces high levels of suPAR in the circulation, drawn as ribbon structures of suPAR and of its D2D3 fragment. These reach the glomerulus, where suPAR and D2D3 bind alpha-v-beta-3 integrin on the podocyte alongside alpha-3-beta-1 integrin and uPAR, with high-fat diet, autoantibodies such as anti-CD40, and APOL1 risk variants listed as synergistic factors. The result is podocyte injury and effacement, loss of filtration integrity and proteinuria, raising the risk of chronic kidney disease. They also reach the tubules, where suPAR and D2D3 bind alpha-v-beta-6, alpha-6-beta-1 and alpha-3-beta-1 integrins on tubular epithelial cells, with intravenous contrast, hypoxia, sepsis and ischemia-reperfusion as synergistic factors. Renal tubular cells show increased energy demand, ATP production, mitochondrial superoxide generation and injury sensitization, raising the risk of acute kidney injury.
Figure 3A How circulating suPAR reaches the kidney. suPAR and its D2D3 fragment bind integrins on the podocyte and on tubular epithelial cells. At the podocyte the result is lost filtration integrity, which shows up as protein in the urine; at the tubule, the cell's energy demand rises. The synergistic factors listed at each site decide which path dominates. Panels B and C of the published figure, covering the pancreatic beta cell and the vasculature, are not shown. Adapted from Reiser J, Hayek SS, Sever S. J Clin Invest. 2026;136(1):e197141, under CC BY 4.0. Select the figure for full resolution.

Papers by topic

  • 62 COVID-19 & Critical Illness
  • 52 suPAR & Inflammatory Biomarkers
  • 51 Vascular Biology, Atherosclerosis & Prevention
  • 35 Nephrology & Cardiorenal
  • 14 Heart Failure & Cardiomyopathy
  • 11 Basic & Mechanistic Science

A paper can count under more than one topic.

02

Cardio-Oncology

Patients with cancer often carry cardiovascular risk before treatment starts, and the treatment can add to it. We work out which patients are at risk, how to catch injury early, and how to treat it without taking effective cancer therapy away.

This is now the lab's largest program. Its main focus is immune-checkpoint-inhibitor myocarditis: registry-based diagnosis and prognosis, troponin and electrocardiogram predictors, severity scoring, and the thymus biology behind susceptibility. We also study anthracycline cardiotoxicity, CAR T-cell cytokine-release cardiomyopathy, and the cardiovascular care of patients undergoing hematopoietic stem cell transplantation. In those patients, atrial fibrillation after transplant is an early warning of systemic vulnerability rather than a transient nuisance.

Lines of work

  • Immune-checkpoint-inhibitor myocarditis: diagnosis, biomarkers, outcomes
  • Anthracycline cardiotoxicity and cardioprotection
  • CAR T-cell and cellular-therapy cardiotoxicity
  • Cardiovascular care in stem cell transplantation
  • Biomarkers in cancer survivors
  • Building the cardio-oncology workforce
Horizontal bar chart ranking predictors of cardiovascular events after haematopoietic stem cell transplantation by variable importance. In decreasing order: anthracycline use, coronary artery disease, transplant type, age, left ventricular ejection fraction of 50 percent or below, race, creatinine, heart failure, diabetes, kidney disease, body mass index, hypertension, triglycerides, and peripheral artery disease.
Figure 1 What predicts cardiovascular events after stem cell transplantation, ranked in the 2,435-patient CARE-BMT derivation cohort. Anthracycline exposure, coronary artery disease and transplant type outrank most traditional cardiovascular risk factors. Adapted from Vasbinder A, et al. J Am Heart Assoc. 2024;13(1):e033599, under CC BY-NC 4.0. Select the figure for full resolution.

How we work

Cohorts and biospecimens on one side, mechanism on the other.

Methods

  • Clinical cohort and registry studies
  • Biomarker discovery and validation
  • Biostatistics and machine learning
  • Multi-omics integration
  • Mechanistic and translational models
  • Health systems and implementation science

Cohorts and registries

  • Emory Cardiovascular Biobank
  • CRIC
  • MESA
  • BARI 2D
  • International Immune Checkpoint Inhibitor Myocarditis Registry
  • CARE-BMT
  • Mi-CARD
  • STOP-COVID
  • Michigan Medicine COVID-19 Cohort (M2C2)
  • ISIC
  • AHA COVID-19 CVD Registry
  • UK Biobank

100,000+ biospecimens assayed across the lab's cohorts and registries.

Browse all 225 publications

Who makes it possible

Funding and collaborators.

Funding support

Federal
  • National Heart, Lung, and Blood Institute, NIH
  • National Institute of Diabetes and Digestive and Kidney Diseases, NIH
Institutional
  • University of Texas Medical Branch
  • Michigan Institute for Clinical and Health Research
  • Frankel Cardiovascular Center, University of Michigan
  • Michigan Alzheimer's Disease Center
Industry
  • Gilead Sciences

Collaborating institutions

  • Emory University
  • University of Michigan
  • University of Washington
  • University of Houston
  • Massachusetts General Hospital
  • Oregon Health & Science University
  • UPMC Sorbonne Universités

Our research spans cardiology, oncology, nephrology, immunology, and data science, and almost none of it is done alone.