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November 16, 1998Circulation Research241 citations

Upregulation of Angiotensin II Type 2 Receptor in Human Heart With Interstitial Fibrosis

Angiotensin II Type 2 Receptor Is Upregulated in Human Heart With Interstitial Fibrosis, and Cardiac Fibroblasts Are the Major Cell Type for Its Expression

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Key result

AT2-R expression was markedly upregulated in dilated cardiomyopathy hearts (3.5-fold protein and 3.1-fold mRNA increase), primarily localizing to interstitial fibroblasts to inhibit mitogen signals.

Authors

YTYoshiaki TsutsumiHMHiroaki MatsubaraNONaohiko Ohkubo

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Overview

AT2-R may represent an antifibrotic target in DCM; extends animal data to human fibroblast localization.

Key Points

  • This research aims to clarify the expression pattern of the angiotensin II type 2 receptor in human left ventricles related to fibrosis in heart failure.
  • Analyzed protein and mRNA expression levels of angiotensin II type 2 receptor in cardiac tissues from failing hearts due to various causes.
  • Evaluated biochemical responses to angiotensin II using LV samples from patients with acute and old myocardial infarction and dilated cardiomyopathy.
  • Assessed localization of receptor expression and corresponding mitogen-activated protein kinase activation in cardiac fibroblasts.
  • AT2-R expression increased significantly in dilated cardiomyopathy hearts by 3.5-fold at protein and 3.1-fold at mRNA levels compared to other heart failure types.
  • Attenuation of AT1-R-mediated inositol phosphate production was noted in failing hearts, while AT2-R in fibroblasts inhibited angiotensin II-induced signal transduction.
  • Collagen type 1 accumulation was much more pronounced in dilated cardiomyopathy compared to old myocardial infarction.

Study Design

Type

Observational

PICO

P
Population
Heart failure (myocardial infarction, dilated cardiomyopathy)
O
Primary Outcome
AT1-R and AT2-R expression at protein, mRNA, and cellular levels

Cite This Study

Tsutsumi et al. (1998) conducted an observational in Heart failure (myocardial infarction, dilated cardiomyopathy). AT2-R expression was markedly upregulated in dilated cardiomyopathy hearts (3.5-fold protein and 3.1-fold mRNA increase), primarily localizing to interstitial fibroblasts to inhibit mitogen signals.

synapsesocial.com/papers/6a15984779ff98d0de4edcd6https://doi.org/10.1161/01.res.83.10.1035
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