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

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Modulation of sarcoplasmic reticulum Ca(2+) cycling in systolic and diastolic heart failure associated with aging

Andrzej M Janczewski1, Edward G Lakatta

  • 1janczewskia@upmc.edu

Heart Failure Reviews
|April 27, 2010
PubMed

Insights

Aging significantly worsens cardiovascular disease, including heart failure (HF). Key changes in cardiac cells involve altered calcium handling and signaling, impacting heart function in older individuals.

Area of Science:

  • Cardiovascular Science
  • Gerontology
  • Molecular Cardiology

Background:

  • Cardiovascular diseases like hypertension and atherosclerosis disproportionately affect older populations, with age being a primary risk factor.
  • Aging leads to detrimental changes in cardiac cell function, including impaired beta-adrenergic receptor (ss-AR) signaling and increased oxidative stress.
  • These cellular changes contribute to the worsening prognosis of cardiovascular conditions in the elderly.

Purpose of the Study:

  • To review age-associated alterations in cardiac calcium (Ca2+) handling proteins and their functional consequences.
  • To explore the role of sarcoplasmic reticulum (SR) Ca2+ transport, sarcolemmal channels, and exchangers in cardiac aging.
  • To discuss sexual dimorphism and cardiac self-renewal in the context of aging and heart failure.

Main Methods:

  • Literature review focusing on age-related changes in cardiovascular physiology.
  • Analysis of studies investigating cardiac myocyte and organ-level functional consequences of aging.
  • Examination of research on calcium-transporting proteins, ss-adrenergic receptors, and reactive oxygen species (ROS) in aging hearts.

Main Results:

  • Aging impairs ss-adrenergic receptor (ss-AR) signaling, increases reactive oxygen species (ROS) generation, and alters excitation-contraction (EC) coupling.
  • Key changes include prolonged action potential (AP), delayed intracellular Ca2+ (Ca(i)(2+)) transient, and blunted force-frequency responses.
  • Altered sarcoplasmic reticulum (SR) Ca2+ uptake, storage, and release are central to these age-related cardiac dysfunctions, involving L-type Ca2+ channels (LCC) and Na+-Ca2+ exchangers (NCX).

Conclusions:

  • Age-related changes in Ca2+ handling proteins significantly impact cardiac myocyte and organ function.
  • Understanding these mechanisms is crucial for addressing the epidemic of cardiovascular disease in older adults.
  • Further research into sexual dimorphism and cardiac regeneration may offer new therapeutic avenues for age-related heart failure.

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