Related Experiment Video

Updated: Jul 9, 2026

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

Calcium dysregulation in diabetic cardiomyopathy & heart failure with preserved ejection fraction

Anza Ali1, Vineet M Sharma2, Yuriana Aguilar-Sanchez1,2

  • 1Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX, United States.

Frontiers in Cardiovascular Medicine
|July 8, 2026
PubMed

Insights

Diabetes and heart failure share molecular links, particularly in type 2 diabetes. Insulin resistance impairs heart function, impacting calcium handling proteins and leading to heart failure with preserved ejection fraction. Gene therapy offers potential treatment.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Molecular Biology

Background:

  • Type 2 diabetes (T2D) significantly increases the risk of cardiovascular disease, especially heart failure with preserved ejection fraction (HFpEF).
  • Diabetes-induced cardiomyopathy (DbCM) mechanisms are complex and not fully understood, but insulin resistance is implicated in cardiac impairment.

Purpose of the Study:

  • To review the molecular mechanisms linking diabetes and HFpEF.
  • To elucidate the role of insulin resistance and calcium (Ca2+)-handling proteins in DbCM progression.
  • To discuss current and potential therapeutic strategies for DbCM and HFpEF.

Main Methods:

  • Literature review focusing on molecular pathways in diabetes-induced cardiomyopathy and HFpEF.
  • Analysis of studies on insulin resistance, Ca2+-handling proteins (SERCA2a, RyR2), and cardiac function.
  • Examination of preclinical and clinical trial data for emerging therapies.

Main Results:

  • Insulin resistance contributes to diastolic dysfunction and hypertrophy in the diabetic heart.
  • Impaired function of Ca2+-handling proteins like SERCA2a and RyR2 are key drivers in DbCM development and progression.
  • Adeno-associated virus (AAV)-mediated gene therapies show promise for treating DbCM.

Conclusions:

  • Understanding the molecular interplay between diabetes and HFpEF is crucial for developing effective treatments.
  • Targeting Ca2+ handling pathways and exploring gene therapies represent promising avenues for managing DbCM and HFpEF.
  • Further research is needed to fully understand DbCM and optimize therapeutic interventions.

Keywords:
Ca2+ dysregulationCa2+ handlingHFpEFdiabetic cardiomyopathygene therapy

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