Physiological and pathological cardiac hypertrophy

Ippei Shimizu1, Tohru Minamino2

  • 1Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan; Division of Molecular Aging and Cell Biology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan.

Insights

The heart adapts to increased demand through physiological or pathological hypertrophy. This review details the molecular and cellular mechanisms differentiating these cardiac growth responses.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cellular Biology

Background:

  • The heart requires continuous high energy supply for blood circulation.
  • Cardiac homeostasis is maintained by growth (hypertrophy), angiogenesis, and metabolic plasticity.
  • Cardiac hypertrophy is classified as physiological (normal function) or pathological (dysfunction).

Purpose of the Study:

  • To review key molecules and cellular responses in cardiac hypertrophy.
  • To differentiate between physiological and pathological cardiac hypertrophy.
  • To understand adaptive and maladaptive cardiac remodeling.

Main Methods:

  • Literature review of molecular and cellular mechanisms.
  • Analysis of signaling pathways involved in cardiac growth.
  • Comparison of cellular responses in different hypertrophy types.

Main Results:

  • Physiological hypertrophy occurs during normal growth, pregnancy, and in athletes.
  • Pathological hypertrophy results from stress (hypertension, infarction) and involves fibrosis, capillary rarefaction, and inflammation.
  • Pathological hypertrophy leads to cellular dysfunction, epigenetic changes, and heart failure.

Conclusions:

  • Understanding the molecular basis of cardiac hypertrophy is crucial for differentiating adaptive from maladaptive responses.
  • Key differences in cellular responses and molecular signaling distinguish physiological from pathological cardiac hypertrophy.
  • This review provides insights into mechanisms driving cardiac remodeling and potential therapeutic targets.

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