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The Formin, DIAPH1, is a Key Modulator of Myocardial Ischemia/Reperfusion Injury
Karen M O'Shea1, Radha Ananthakrishnan1, Qing Li1
1Diabetes Research Program, Department of Medicine, New York University Langone Medical Center, New York, NY 10016, USA.
Ebiomedicine
|December 15, 2017
Summary
Diaphanous-related formin 1 (DIAPH1) plays a key role in myocardial ischemia/reperfusion (I/R) injury. Targeting DIAPH1 may offer a new strategy for protecting the heart after infarction.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Signaling
Background:
- Myocardial ischemia/reperfusion (I/R) injury involves complex biochemical and ionic changes.
- The receptor for advanced glycation end-products (RAGE) is implicated in I/R injury.
- DIAPH1, a RAGE-interacting protein, is a potential mediator of cardiac I/R response.
Purpose of the Study:
- To investigate the role of DIAPH1 in experimental myocardial I/R in mice.
- To elucidate the molecular mechanisms by which DIAPH1 influences cardiac I/R injury.
Main Methods:
- Induction of myocardial I/R in wild-type and Diaph1-deleted mice.
- Hypoxia/reoxygenation (H/R) in H9C2 and AC16 cardiac cell lines.
- Assessment of infarct size, contractile function, DIAPH1 expression, actin polymerization, and gene expression.
Main Results:
- Myocardial DIAPH1 expression increased following I/R and H/R.
- Genetic deletion of Diaph1 reduced infarct size and improved cardiac function post-I/R.
- DIAPH1 silencing altered actin polymerization, SR Ca2+ ATPase, and sodium-calcium exchanger expression.
Conclusions:
- DIAPH1 is essential for the cardiac response to I/R injury.
- DIAPH1 modulates key cellular pathways involved in I/R pathogenesis.
- Targeting DIAPH1 presents a potential therapeutic avenue for myocardial salvage.
