Premature Senescence ”Senescence is more than merely a cell division clock that regulates the proliferative lifespan of normal cells. “Premature” senescence is an active cytostaticprogram that is triggered in response to proliferative or genotoxic stress, such as the expression of strong oncogenes, tumor suppressor loss, exposure to DNA damage, and reactivation of tumor suppressor pathways. […]
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JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age A hallmark of aging is chronic sterile inflammation, which is closely associated with frailty and age-related diseases. We found that senescent fat progenitor cells accumulate in adipose tissue with aging and acquire a senescence-associated secretory phenotype (SASP), with increased production of proinflammatory
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Regulation of longevity by FGF21: Interaction between energy metabolism and stress responses. Fibroblast growth factor 21 (FGF21) is a hormone-like member of FGF family which controls metabolic multiorgan crosstalk enhancing energy expenditure through glucose and lipid metabolism. In addition, FGF21 acts as a stress hormone induced by endoplasmic reticulum stress and dysfunctions of mitochondria and
Klotho is a transmembrane protein that, in addition to other effects, provides some control over the sensitivity of the organism to insulin and appears to be involved in ageing. Its discovery was documented in 1997 by Makoto Kuro-o et al.[9] The name of the gene comes from Klotho or Clotho, one of the Moirai, or
SIRT1 stands for sirtuin (silent mating type information regulation 2 homolog) 1 (S. cerevisiae), referring to the fact that its sirtuinhomolog (biological equivalent across species) in yeast (S. cerevisiae) is Sir2. SIRT1 is an enzyme that deacetylates proteins that contribute to cellular regulation (reaction to stressors, longevity).[8] Sirtuin 1 is a member of the sirtuin
FOXO3 belongs to the O subclass of the forkhead family of transcription factorswhich are characterized by a distinct fork head DNA-binding domain. There are three other FoxO family members in humans, FOXO1, FOXO4 and FOXO6. These transcription factors share the ability to be inhibited and translocated out of the nucleus on phosphorylation by proteins such
interstellar 88/8 EIGHT CYCLE 32 DAY CHALLENGE Lose 60lbs in 32 days and WIN $1000 in INTERSTELLAR BLENDS *Sound impossible? It’s not. Multiple people have already achieved this and greater and there’s time stamped pictures in group authenticating it. The current record is 66 lbs in 32 days set by Bev Beyer on April 18th,
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Autophagy (or autophagocytosis) (from the Ancient Greek αὐτόφαγος autóphagos, meaning “self-devouring”[1] and κύτος kýtos, meaning “hollow”[2]) is the natural, regulated mechanism of the cell that removes unnecessary or dysfunctional components.[3] It allows the orderly degradation and recycling of cellular components.[4][5] Three forms of autophagy are commonly described: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). In macroautophagy, expendable cytoplasmic constituents are targeted and isolated from the rest of the cell within a
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“5′ AMP-activated protein kinase or AMPK or 5′ adenosine monophosphate-activated protein kinase is an enzyme (EC 2.7.11.31) that plays a role in cellular energy homeostasis, largely to activate glucose and fatty acid uptake and oxidation when cellular energy is low. It belongs to a highly conserved eukaryoticprotein family and its orthologues are SNF1 and SnRK1
MTOR: The Rapid Aging Pathway “The mammalian target of rapamycin(mTOR), also known as the mechanistic target of rapamycin and FK506-binding protein 12-rapamycin-associated protein 1 (FRAP1), is a kinase that in humans is encoded by the MTOR gene.[5][6][7] mTOR is a member of the phosphatidylinositol 3-kinase-related kinase family of protein kinases.[8] mTOR links with other proteins
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