# CD37 as a Regulator of Platelet Patho(Physiological) Responses

> **NIH NIH R01** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2024 · $579,849

## Abstract

SUMMARY
Eighty-five percent (85%) of cardiovascular disease deaths occur due to either myocardial infarction (MI) or
stroke, platelet-driven events. While antiplatelet therapy for secondary CVD prevention is well-established,
antiplatelet therapy is not commonly prescribed to prevent a first MI or stroke as the cardioprotective benefits
are offset by major bleeding risk. The well-established role of platelets in the pathogenesis of MI and stroke and
the lack of platelet-directed therapeutic options for primary CVD prevention necessitates investigating novel
platelet targets which would impact the multifaceted effects of platelets without impacting hemostasis.
Furthermore, while platelets were once considered primarily mediators of hemostasis and thrombosis, it is now
understood that they play an important role as immune mediators. Platelets play central roles in the chronic
inflammation that fuels atherosclerosis, from the initial innate immune response to damage-associated molecular
pattern proteins to the engagement of adaptive immunity. To effectively target this axis, a better understanding
of the pathways and cell-cell communication networks by which platelets promote atherogenesis and inhibit
inflammation resolution in CVD Is required.
By unbiased platelet sequencing, we have identified a novel regulator of platelet activation responses, CD37.
This proposal aims to understand how CD37 regulates platelet functional responses and how targeting platelet
CD37 may be a viable therapeutic approach to reduce (patho)physiological platelet responses.
In Aim 1 we will establish the role of CD37 in platelet activation responses and identify protein-binding partners
in CD37-enriched membrane microdomains. Aim 2 will assess if targeting platelet CD37 alters atherosclerosis
and plaque stability. The studies will serve as an essential foundation to demonstrate the viability of targeting
platelet CD37 to reduce thrombosis, atherogenesis, and systemic inflammation. If our hypotheses prove
accurate, CD37, our newly identified platelet activity gene, could be targeted to prevent and treat a wide variety
of platelet-mediated disorders, including cardiovascular disease.

## Key facts

- **NIH application ID:** 10884199
- **Project number:** 5R01HL167917-02
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Tessa Barrett
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $579,849
- **Award type:** 5
- **Project period:** 2023-07-15 → 2028-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10884199

## Citation

> US National Institutes of Health, RePORTER application 10884199, CD37 as a Regulator of Platelet Patho(Physiological) Responses (5R01HL167917-02). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10884199. Licensed CC0.

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