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November 22, 2017EBioMedicineOpen Access

The Formin, DIAPH1, is a Key Modulator of Myocardial Ischemia/Reperfusion Injury

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Key result

Genetic deletion of Diaph1 reduced infarct size and improved contractile function after myocardial ischemia/reperfusion in mice compared to wild-type controls.

Why the study?

Does genetic deletion or silencing of Diaph1 reduce infarct size and improve contractile function in experimental models of myocardial ischemia/reperfusion injury?

Population

Wild-type mice, Diaph1 knockout mice, and H9C2 and AC16 cell lines subjected to experimental myocardial…

Comparison

Genetic deletion or silencing of Diaph1 vs Wild-type mice or control cells

Design

Preclinical

Authors

KOKaren M. O’SheaUniversity of Maryland, BaltimoreRARadha AnanthakrishnanINHS AsviniQLQing LiChinese Academy of Tropical Agricultural Sciences

Discussion

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Overview

Diaph1 deletion attenuates ischemia/reperfusion injury in mice; hypothesis-generating and leaves open translational potential in humans.

Structured PICO

Does genetic deletion or silencing of Diaph1 reduce infarct size and improve contractile function in experimental models of myocardial ischemia/reperfusion injury?

P
Population
Wild-type mice, Diaph1 knockout mice, and H9C2 and AC16 cell lines subjected to experimental myocardial ischemia/reperfusion (I/R) or hypoxia/reoxygenation (H/R)
I
Intervention
Genetic deletion or silencing of Diaph1
C
Comparator
Wild-type mice or control cells
O
Outcome
Infarct size and contractile function after I/Rsurrogate

Genetic deletion of DIAPH1 reduces infarct size and improves contractile function in experimental myocardial ischemia/reperfusion injury, highlighting it as a potential therapeutic target.

Cite This Study

O’Shea et al. (2017) studied Myocardial ischemia/reperfusion injury. Genetic deletion or silencing of Diaph1 vs. Wild-type mice / control cells was evaluated on Infarct size and contractile function. Genetic deletion of Diaph1 reduced infarct size and improved contractile function after myocardial ischemia/reperfusion in mice compared to wild-type controls.

synapsesocial.com/papers/6a205aea3b3f5eb7b098fa9ehttps://doi.org/10.1016/j.ebiom.2017.11.012
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.1990 · 2,883 citations
  2. 2Altered calcium regulation in isolated cardiomyocytes from Egr-1 knock-out mice2013 · 18 citations
  3. 3Increased Expression of Cytoskeletal, Linkage, and Extracellular Proteins in Failing Human Myocardium2000 · 326 citations
  4. 4Recovery of Ventricular Function after Myocardial Infarction in the Reperfusion Era: The Healing and Early Afterload Reducing Therapy Study2001 · 215 citations
  5. 5Sodium-Calcium Exchange: A Molecular Perspective2000 · 552 citations