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Calcium, Cell Function and Cell Death

  • Louis V. Avioli
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 208)

Abstract

The nature of the biologic mechanism(s) which initiate and perpetuate the aging process is still under intensive investigation. Although those with vested interests in “aging research” would agree that the programming of the aging phenomenon is related to specific acquired and/or genetic molecular dysfunctions which condition DNA and protein synthesis, and post-translational events in cells, the fundamental “trigger” mechanism(s) which activates mammalian senescence has yet to be discovered. A number of theories have been promulgated to account for the molecular cellular dysfunctions which attend the senescent process. These include: (a) alterations in host-defense systems and cell-mediated immunity; (b) progressive accumulations of circulating “toxic” substances which damage DNA; (c) an acquired inability to destroy “free-radicals”, the latter resulting in the cellular accumulation of superoxide and hydrogen peroxide type reactants and a gradual decline in cellular integrity; (d) cellular “commitment” theories which stress programmed aging and finite replicative life-span of cells; and (e) gradual alterations in those mechanisms which regulate cytosolic calcium concentration resulting in molecular disarray, decrease in, cellular viability and cell death.

Keywords

Cystic Fibrosis Amyotrophic Lateral Sclerosis Parathyroid Hormone Vascular Smooth Muscle Cell Cytosolic Calcium Concentration 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • Louis V. Avioli
    • 1
  1. 1.Division of Bone and Mineral DiseasesWashington University School of MedicineSt. LouisUSA

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