Calcium Signaling and Cardiac Adaptation to Stress: Focus on Pregnancy and Diabetes

Sathya Velmurugan1, Sanda Despa2

  • 1Department of Internal Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Kentucky, Lexington, KY 40536, USA.

Biomolecules
|October 29, 2025
PubMed

Insights

Calcium (Ca2+) signaling is vital for heart function during pregnancy and diabetes. Understanding these pathways can reveal new therapeutic targets for cardiac health in these conditions.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Signaling
  • Endocrinology

Background:

  • Calcium (Ca2+) signaling is essential for cardiac function, regulating contractility, excitability, and metabolism.
  • Cardiac adaptation to stress involves complex Ca2+ signaling pathways.
  • Pregnancy and diabetes represent distinct physiological and pathophysiological states impacting cardiac Ca2+ handling.

Purpose of the Study:

  • To review the role of Ca2+ signaling in cardiac adaptation during pregnancy.
  • To examine the pathological maladaptation of cardiac Ca2+ signaling in diabetes.
  • To identify shared Ca2+-dependent mechanisms in cardiac hypertrophy, energy imbalance, and electrical remodeling under these conditions.

Main Methods:

  • Literature review focusing on Ca2+ signaling in cardiac physiology and pathology.
  • Analysis of studies investigating cardiac adaptation to pregnancy.
  • Examination of research on cardiac dysfunction in diabetes mellitus.

Main Results:

  • Ca2+ signaling plays a critical role in physiological cardiac adaptation to pregnancy.
  • Dysregulated Ca2+ signaling contributes to cardiac maladaptation in diabetes.
  • Shared pathways in hypertrophy, energy imbalance, and electrical remodeling are implicated in both conditions.

Conclusions:

  • Understanding Ca2+ signaling mechanisms is crucial for addressing cardiac issues in pregnancy and diabetes.
  • Identifying common signaling pathways may reveal novel therapeutic targets.
  • Further research is needed to bridge knowledge gaps in cardiac Ca2+ regulation.

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