The mechanisms which are incorporated into the flow chart include:
-- Nonenzymatic glycation of long-lived proteins and nuclear DNA.
-- Accumulation of mutations in the mitochondrial genomes of postmitotic cells.
-- Increasing acetylation of histones opens heterochromatin, permitting inappropriate expression of aging-specific genes.
-- Accumulation of lipofuscin in lysosomes of postmitotic cells.
-- Redox stress from Reactive Oxidative Species (ROS or Free Radicals) causes both oxidative damage
to macromolecules and increased redox potential. Increased redox potential alters some intracellular
signaling pathways and alters some enzyme activities.
-- Damage and crosslinking to long-lived macromolecules in postmitotic cells and extracellular matrix.
-- Telomere shortening induces altered phenotype and a halt in cell division in some cells.
-- Apoptosis, necrosis, and cell loss leading to tissue wasting and organ malfunction.
-- Alterations in neuroendocrine and immune systems.
-- Decline in rate of repair and turnover of macromolecules and organelles.
-- Export of toxic reactive species and cytokines from senescent cells.
-- Induction of cancer.
This flow chart will be maintained on the Worldwide Web as a reference to researchers, and will be updated as new information comes to light.
http://www.LegendaryPharma.com/senescence.html#Mechanisms
Key words:
senescence, aging, biochemistry, flowchart, causes
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