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Updated: Jan 20, 2026

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
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Gender Differences in Cardiac Hypertrophy.

Jian Wu1, Fangjie Dai2, Chang Li2

  • 1Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, 180 Feng Lin Road, Shanghai, 200032, China. wu.jian@zs-hospital.sh.cn.

Journal of Cardiovascular Translational Research
|August 17, 2019
PubMed
Summary
This summary is machine-generated.

Sex hormones significantly influence cardiac hypertrophy, with estrogen offering protection in females, a benefit lost post-menopause. Understanding these sexual dimorphisms is key for targeted heart failure therapies.

Keywords:
GenderPathological cardiac hypertrophyPhysiological cardiac hypertrophyPressure overloadVolume overload

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Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Molecular Cardiology

Background:

  • Cardiac hypertrophy is an adaptive response to stress, classified as concentric or eccentric based on the stimulus.
  • Females generally exhibit a more favorable hypertrophy response than males, yet it poses a greater heart failure risk.
  • Hormonal influences, particularly estrogen and androgens, play critical roles in sex-based differences in cardiac hypertrophy.

Purpose of the Study:

  • To review current understanding of sexual dimorphisms in cardiac hypertrophy.
  • To highlight recent advances in the molecular mechanisms of sex hormone regulation in cardiac hypertrophy.
  • To explore potential gender-oriented therapeutic strategies for pathological hypertrophy.

Main Methods:

  • Literature review and synthesis of existing research on cardiac hypertrophy and sex hormones.
  • Analysis of molecular signaling pathways involved in sex hormone-mediated cardiac remodeling.
  • Discussion of clinical implications for gender-specific treatment approaches.

Main Results:

  • Estrogen provides a protective effect against cardiac hypertrophy, counteracting pro-hypertrophic pathways.
  • Androgens generally promote cardiac hypertrophy, opposing estrogen's effects.
  • Menopausal status significantly alters estrogen's protective role, impacting cardiovascular risk.

Conclusions:

  • Sex hormones are critical regulators of cardiac hypertrophy, exhibiting significant sexual dimorphism.
  • Understanding the molecular interplay of sex hormones is essential for developing effective, gender-specific treatments for heart failure.
  • Further research into hormonal networks may unlock novel therapeutic avenues for pathological cardiac hypertrophy.