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February 9, 2013Circulation Heart Failure

Bidirectional Regulation of Nuclear Factor-κB and Mammalian Target of Rapamycin Signaling Functionally Links Bnip3 Gene Repression and Cell Survival of Ventricular Myocytes

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Population

Ventricular myocytes

Design

Preclinical

Authors

RDRimpy DhingraSt. Boniface HospitalHGHongying GangSt. Boniface HospitalYWYan WangSouth China Agricultural University

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Overview

Hypothesis-generating for mTOR-Bnip3 modulation in ischemic myocyte death; leaves open therapeutic targeting pending human validation.

Structured PICO

P
Population
Ventricular myocytes
I
Intervention
Modulation of NF-κB and mTOR signaling (IKKβ overexpression, mTOR overexpression, rapamycin inhibition)
O
Outcome
Ventricular myocyte survival and Bnip3 expressionsurrogate

Demonstrates a bidirectional link between NF-κB signaling and mTOR that regulates Bnip3 expression and cardiac myocyte death, highlighting a potential cardioprotective target during ischemia.

Cite This Study

Dhingra et al. (2013) studied this question.

synapsesocial.com/papers/6a766b0fee08d608e595c414https://doi.org/10.1161/circheartfailure.112.000061
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Also Consider

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

  1. 1Nuclear Factor-κB–Mediated Cell Survival Involves Transcriptional Silencing of the Mitochondrial Death Gene BNIP3 in Ventricular Myocytes2005 · 99 citations
  2. 2Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice2007 · 307 citations
  3. 3Akt Signaling and Growth of the Heart2006 · 117 citations
  4. 4Cardiomyocyte NF-κB p65 promotes adverse remodelling, apoptosis, and endoplasmic reticulum stress in heart failure2010 · 252 citations
  5. 5Inducible Expression of BNIP3 Provokes Mitochondrial Defects and Hypoxia-Mediated Cell Death of Ventricular Myocytes2002 · 318 citations