4.7 Review

Altered Ca2+ sparks in aging skeletal and cardiac muscle

Journal

AGEING RESEARCH REVIEWS
Volume 7, Issue 3, Pages 177-188

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2007.12.003

Keywords

Excitation-contraction coupling; Calcium sparks; Aging; Heart failure; Cardiomyopathy; Skeletal muscle; Cardiac muscle

Funding

  1. NHLBI NIH HHS [R01 HL069000-06, R01 HL069000] Funding Source: Medline
  2. NIA NIH HHS [R01 AG028614-03, R01 AG028856-01A2, R01 AG028856, R01 AG015556-10, R01 AG015556, R01 AG028614] Funding Source: Medline
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL069000] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE ON AGING [R01AG015556, R01AG028614, R01AG028856] Funding Source: NIH RePORTER

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Ca2+ sparks are the fundamental units that comprise Ca2+-induced Ca2+ release (CICR) in striated muscle cells. In cardiac muscle, spontaneous Ca2+ sparks underlie the rhythmic CICR activity during heart contraction. In skeletal muscle, Ca2+ sparks remain quiescent during the resting state and are activated in a plastic fashion to accommodate various levels of stress. With aging, the plastic Ca2+ spark signal becomes static in skeletal muscle, whereas loss of CICR control leads to leaky Ca2+ spark activity in aged cardiomyocytes. Ca2+ spark responses reflect the integrated function of the intracellular Ca2+ regulatory machinery centered around the triad or dyad junctional complexes of striated muscles, which harbor the principal molecular players of excitation-contraction coupling. This review highlights the contribution of age-related modification of the Ca2+ release machinery and the effect of membrane structure and membrane cross-talk on the altered Ca2+ spark signaling during aging of striated muscles. (c) 2008 Elsevier Ireland Ltd. All rights reserved.

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