# Novel Molecular Mechanisms of Programmed Necrosis

> **NIH NIH R01** · TEMPLE UNIV OF THE COMMONWEALTH · 2020 · $390,000

## Abstract

PROJECT SUMMARY
Approximately 7.6 m Americans currently suffer the burden of myocardial infarction (MI) and there are ~1
million new and recurrent MIs each year resulting in immediate death in some individuals and a
predisposition to heart failure (HF) in survivors. Given that necrosis is the major type of cell death in the
heart during MI and drives the gradual loss of cells associated with the progression of HF, defining the
molecular mechanisms underlying necrosis will offer novel treatment strategies for cardiovascular disease
and numerous other death-driven disorders. The current proposal is designed to define the role of N-
ethylmaleimide sensitive factor (NSF gene) in programmed necrosis. NSF encodes an ATPase that is
required for SNARE-mediated membrane fusion events. Here we provide preliminary data that NSF plays a
significant role in membrane rupture and programmed necrosis. This proposal will examine the centrality of
NSF in cellular pathways involved in programmed necrosis and using genetic gain- and loss-of-function
strategies evaluate the contribution of NSF to myocardial ischemia-reperfusion injury and the progression of
heart failure resulting from diverse etiologies. The ultimate goal of these studies is to develop novel
therapeutic strategies with translational potential.

## Key facts

- **NIH application ID:** 9857639
- **Project number:** 5R01HL136954-04
- **Recipient organization:** TEMPLE UNIV OF THE COMMONWEALTH
- **Principal Investigator:** John William Elrod
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $390,000
- **Award type:** 5
- **Project period:** 2017-04-01 → 2021-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9857639

## Citation

> US National Institutes of Health, RePORTER application 9857639, Novel Molecular Mechanisms of Programmed Necrosis (5R01HL136954-04). Retrieved via AI Analytics 2026-07-15 from https://api.ai-analytics.org/grant/nih/9857639. Licensed CC0.

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