Cellular Mechanism in Aging

Cellular Senescence is the aftereffect of a dynamic decrease in the proliferative limit and life expectancy of cells and the impacts of continuous exposure to exogenous influence that outcome in the the progressive accumulation of cellular and molecular damage. Mechanism of Cellular Aging includes numerous Cellular, Molecular, Biochemical pathways. Various cellular function declines continuously with age.  Oxidative phosphorylation by mitochondria is decreases, as is synthesis of nucleic acids and structural and enzymatic proteins, cell receptors, and Transcription factors.  Senescent cells have a diminished limit with respect to take-up of nutrient and for repair of chromosomal damage. There are many  morphological modifications in aging cell includes irregular a lobed nuclei, pleomorphic vacuolated mitochondria, diffused endoplasmic reticulum, loss of cytoplasmic content, and distored  Golgi apparatus. Concomitantly, there is a steady accumulation of the pigment lipofuscin, represents a product of lipid peroxidation and evidence of oxidative damage; advanced glycation end products, which result from non-enzymatic glycosylation and are capable of cross-linking adjacent proteins; and the accumulation of abnormally folded proteins.

  • Decline in protein synthesis
  • Stiffening in collagen
  • Decline in energy production
  • Change in fluidity and permeability of plasma membrane
  • Decrease in granular endoplasmic reticulum
  • Degeneration of chloroplast
  • Mutation in mitochondrial DNA
  • Loss of ribosomal RNA
  • Decline in transcription
  • Decline translation
  • DNA scaffolding
  • DNA oxidation
  • Follicular stem cell aging
  • Follicular stem cell aging

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