Hayek Lab University of Texas Medical Branch

We find the signal
before the damage.

Inflammation injures the heart, the kidney, and the metabolic system together. The Hayek Lab works out which molecules carry that injury between organs, turns them into biomarkers clinicians can act on, and applies them where the risk is highest, from chronic kidney disease to patients being treated for cancer.

The research Work with us
Peer-reviewed publications
225
Citations
27,000+
Research funding
$10M+
Lab members, past and present
51

What we do

Two programs, one question: what does inflammation cost the patient in front of us?

01

Inflammation and Cardiovascular-Kidney-Metabolic Disease

The heart, the kidney, and metabolism fail together, and inflammation is the common thread. We study the immune signals that carry injury from one organ to another, and we translate them into biomarkers clinicians can act on.

  • suPAR and the kidney: incident CKD, eGFR decline, AKI, and 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
Read the full program

02

Cardio-Oncology

Cancer therapy saves lives and injures hearts. We work out which patients are at risk, how to detect that injury early, and how to treat it without taking effective cancer therapy away.

  • Immune-checkpoint-inhibitor myocarditis: diagnosis, biomarkers, outcomes
  • Anthracycline cardiotoxicity and cardioprotection
  • CAR T-cell and cellular-therapy cardiotoxicity
  • Cardiovascular care in stem cell transplantation
Read the full program

The idea

A molecule that injures organs it never touched.

How suPAR carries injury from one organ to another Membrane-bound uPAR on myeloid, endothelial and vascular smooth muscle cells drives local inflammation and tissue remodeling. Cleavage releases soluble suPAR into the bloodstream, where it acts on distant targets through the alpha-v beta-3 integrin and RAGE receptors, injuring the kidney, the vasculature and metabolic tissue. Membrane uPAR Local inflammation, remodeling Cleavage Soluble suPAR in the blood Kidney Vasculature Metabolic Distant injury via αvβ3 · RAGE
One receptor, two modes. Membrane uPAR injures the tissue it sits in; once cleaved, suPAR travels and injures organs it never touched. Adapted from Reiser, Hayek & Sever, J Clin Invest 2026 and Hayek & Dryer, Circulation Research 2026.

Signature work

A decade establishing suPAR as a cross-organ driver of disease.

  1. 2015 Discovery

    Soluble Urokinase Receptor and Chronic Kidney Disease

    The New England journal of medicine First author

  2. 2017 Mechanism

    A tripartite complex of suPAR, APOL1 risk variants and αvβ3 integrin on podocytes mediates chronic kidney disease

    Nature medicine First author

  3. 2020 Generalization

    Soluble Urokinase Receptor and Acute Kidney Injury

    The New England journal of medicine First author

  4. 2022 Causation

    Increased soluble urokinase plasminogen activator levels modulate monocyte function to promote atherosclerosis

    Journal of Clinical Investigation Senior author

  5. 2026 Synthesis

    uPAR/suPAR Signaling and Organ Crosstalk in Cardiovascular-Kidney-Metabolic Syndrome

    Circulation Research First author

All 225 publications

Latest

What is happening now.

Eight members of the Hayek Lab outdoors by the water in Galveston

Physicians, scientists, and trainees.

51 people have worked in this lab, in Galveston and, before it, in Ann Arbor. Meet the team.

Work with us

We collaborate with academic groups, health systems, and industry partners.

Biomarker validation, ancillary studies to ongoing trials, and registry-based outcomes research. If you have a cohort, an assay, or a compound and a cardiovascular question, we are interested.

Partner with the lab Support the work

Gifts fund pilot studies and biospecimen collection. To direct one to this lab, contact UTMB Development or write to us.