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Crim1 suppresses left ventricular hypertrophy.

Long Yang1, Jionghong He1, Guiling Xia1

  • 1Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.

Biomedical Reports
|July 2, 2019
PubMed
Summary

Cysteine-rich transmembrane bone morphogenetic protein regulator 1 (Crim1) suppresses ventricular hypertrophy. Inhibiting angiotensin receptor type 1 (AT1R) increases Crim1, offering a new therapeutic target for cardiac hypertrophy.

Keywords:
abdominal aortic coarctationcysteine-rich transmembrane bone morphogenetic protein regulator 1left ventricular hypertrophytelmisartan

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Regenerative Medicine

Background:

  • Left ventricular hypertrophy (LVH) is a major risk factor for heart failure and sudden cardiac death.
  • Cysteine-rich transmembrane bone morphogenetic protein regulator 1 (Crim1) is crucial for heart development and highly expressed in cardiac tissue.
  • The precise role of Crim1 in regulating ventricular hypertrophy remains to be elucidated.

Purpose of the Study:

  • To investigate the hypothesis that Crim1 exerts an inhibitory effect on ventricular hypertrophy.
  • To explore the relationship between angiotensin receptor type 1 (AT1R) inhibition and Crim1 expression.
  • To evaluate Crim1's potential as a therapeutic target for cardiac hypertrophy.

Main Methods:

  • Primary rat ventricular myocytes were subjected to mechanical stretch to induce hypertrophy, followed by treatment with telmisartan or Ad-Crim1.
  • Rat ventricular hypertrophy was induced via abdominal aortic coarctation (AAC) and treated with telmisartan, Ad-Crim1, or an empty adenovirus vector.
  • Crim1 expression levels were assessed in hypertrophic and control conditions.

Main Results:

  • Crim1 expression was found to be downregulated in hypertrophic ventricles.
  • Telmisartan treatment significantly upregulated Crim1 expression in the left ventricle, both in vitro and in vivo.
  • Overexpression of Crim1 via Ad-Crim1 infection or telmisartan treatment effectively inhibited both in vitro and in vivo ventricular hypertrophy.

Conclusions:

  • Crim1 demonstrates a significant suppressive function against ventricular hypertrophy.
  • Modulating Crim1 expression presents a novel therapeutic strategy for treating cardiac hypertrophy.
  • Targeting Crim1 may offer a new avenue for managing heart failure and sudden death associated with LVH.