Pathology II Flashcards
Genetically programmed like apoptosis and morphologically/biochemically resembles necrosis
Necroptosis
However, in necroptosis, we do not have any
Caspase activation
The typical ligand for necroptosis is
TNFR1
Ligation then recruits
RIP1 and RIP3
Terminal events include membrane permeabilization, ROS, mitochondria damage, decreased ATP
Necroptosis
A survival mechanism under stress conditions, especially nutrient deprivation
Autophagy
Selective and regulated by greater than a dozen proteins
Autophagy
The result of a progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of cellular and molecular damage due to the effects of exposure to exogenous influences
Cellular aging
Damage directly to DNA
–Decreasing effectivity of DNA repair enzymes
–Possible contribution of free radical insults
Accumulating DNA damage
Cellular aging shows a reduced capacity of the cell to
Divide
This reduced capacity to divide is the result of progressive shortening of telomere ends without activation of
Telomerase to repair them
Reduced translation of proteins and defective activity of chaperones, proteasomes, and repair enzymes
Defective protein homeostasis seen in cellular aging
Some environmental stresses counteract aging. An example of this is a
30% reduction in calories
rare disease that causes premature aging
Progeria
The most common cause of death in progeria
Atherosclerosis
A genetic disease, but it usually occurs sporadically and does not run in families
Progeria
Unlike some other diseases of premature aging that are due to problems with DNA repair, such as Werner syndrome, progeria is due to a mutation in the gene coding for
Prelamin A