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June 29, 2009Clinical and Experimental Pharmacology and Physiology

Downregulation of survival signalling pathways and increased apoptosis in the transition of pressure overload‐induced cardiac hypertrophy to heart failure

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Key result

Transverse aortic constriction in mice induced early concentric and late eccentric hypertrophy with LV dysfunction, associated with downregulated survival signaling and increased apoptosis.

Population

Mice subjected to transverse aortic constriction (TAC) or sham operation

Comparison

Transverse aortic constriction for 1-16 weeks vs Sham operation

Design

Preclinical

Follow-up

1 to 16 weeks

Authors

XLXiaomei LiYMYi‐Tong MaYYYi‐Ning Yang

Discussion

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Member takes

Overview

Supports survival signaling downregulation as HF transition mechanism in pressure overload; hypothesis-generating, requires translational validation before clinical consideration.

Structured PICO

P
Population
Mice subjected to transverse aortic constriction or sham operation for 1-16 weeks to study the transition from compensated hypertrophy to heart failure.
I
Intervention
Transverse aortic constriction (TAC) for 1-16 weeks
C
Comparator
Sham operation
O
Outcome
Temporal relationship between cardiomyocyte apoptosis and survival signalling (ERK1/2, Akt, GSK-3beta) in the transition from hypertrophy to heart failuresurrogate

Downregulation of survival signaling pathways (ERK1/2, Akt, GSK3beta) and increased apoptosis are key mechanisms in the transition from compensated cardiac hypertrophy to heart failure in a pressure-overload mouse model.

Cite This Study

Li et al. (2009) studied pressure overload-induced cardiac hypertrophy to heart failure. Transverse aortic constriction (TAC) vs. sham operation was evaluated on LV dimensions, contractile function, and molecular markers of apoptosis and survival signaling. Transverse aortic constriction in mice induced early concentric and late eccentric hypertrophy with LV dysfunction, associated with downregulated survival signaling and increased apoptosis.

synapsesocial.com/papers/6a7c97841c02bd024a6ee22bhttps://doi.org/10.1111/j.1440-1681.2009.05243.x
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Also Consider

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

  1. 1Increased Cardiomyocyte Apoptosis and Changes in Proapoptotic and Antiapoptotic Genes <i>bax</i> and <i>bcl</i> -2 During Left Ventricular Adaptations to Chronic Pressure Overload in the Rat1999 · 284 citations
  2. 2Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats1999 · 28 citations
  3. 3Cardiomyocyte loss is not required for the progression of left ventricular hypertrophy induced by pressure overload in female mice2016 · 6 citations
  4. 4Pressure Overload Induces Early Morphological Changes in the Heart2012 · 80 citations
  5. 5Changes in Contractile and Non-Contractile Proteins, Intracellular Ca2+ and Ultrastructures During The Development of Right Ventricular Hypertrophy and Failure in Rats.1992 · 9 citations