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Updated: Feb 10, 2026

Mimicking the Function of Signaling Proteins: Toward Artificial Signal Transduction Therapy
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Mimicking the Function of Signaling Proteins: Toward Artificial Signal Transduction Therapy

Published on: September 29, 2016

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Mechanisms of Cardiovascular Homeostasis and Pathophysiology--From Gene Expression, Signal Transduction to Cellular

Hiroshi Akazawa1

  • 1Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo.

Circulation Journal : Official Journal of the Japanese Circulation Society
|November 6, 2015
PubMed

Insights

This review explores molecular mechanisms in heart disease, focusing on key regulators like Nkx2-5 and signaling pathways. Understanding these cardiac cell processes is crucial for developing new cardiovascular disease therapies.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Pathophysiology

Background:

  • Cardiomyocytes lose proliferative capacity post-birth, growing in size without division.
  • Pathological conditions trigger complex signaling in cardiomyocytes, leading to dysfunction and cell death.
  • Cardiovascular diseases represent a major global health burden, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To summarize approaches for uncovering molecular and cellular pathophysiology in the heart.
  • To highlight key molecular players in cardiac gene regulation, growth, survival, and disease development.
  • To provide insights into mechanisms underlying pathological hypertrophy, remodeling, and atrial fibrillation.

Main Methods:

  • Review of literature focusing on molecular and cellular mechanisms in cardiovascular disease.
  • Examination of the role of specific molecular targets: Nkx2-5, 3-phosphoinositide-dependent kinase-1, angiotensin II type 1 receptor, and mast cells.
  • Analysis of intracellular signaling pathways and intercellular communication networks.

Main Results:

  • Nkx2-5 is critical for transcriptional regulation of the cardiac gene program.
  • 3-phosphoinositide-dependent kinase-1 regulates postnatal cardiomyocyte growth, survival, and function.
  • Angiotensin II type 1 receptor mediates pathological hypertrophy and remodeling.
  • Mast cell infiltration contributes to atrial remodeling and fibrillation.

Conclusions:

  • Elucidating molecular and cellular mechanisms is vital for advancing cardiovascular disease therapies.
  • Targeting specific pathways involving Nkx2-5, PDK-1, AT1R, and mast cells offers potential therapeutic avenues.
  • A comprehensive understanding of cardiac pathophysiology is essential for combating prevalent cardiovascular diseases.

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