AMP-activated protein kinase (AMPK) controls the aging process via an integrated signaling network.

By Antero Salminen, K. Kaarniranta. Ageing Research Reviews, 2012

819 citations recorded by the source corpus.

Efficient control of energy metabolic homeostasis, enhanced stress resistance, and qualified cellular housekeeping are the hallmarks of improved healthspan and extended lifespan. AMPK signaling is involved in the regulation of all these characteristics via an integrated signaling network. Many studies with lower organisms have revealed that increased AMPK activity can extend the lifespan. Experiments in mammals have demonstrated that AMPK controls autophagy through mTOR and ULK1 signaling which augment the quality of cellular housekeeping. Moreover, AMPK-induced stimulation of FoxO/DAF-16, Nrf2/SKN-1, and SIRT1 signaling pathways improves cellular stress resistance. Furthermore, inhibition of NF-κB signaling by AMPK suppresses inflammatory responses. Emerging studies indicate that the responsiveness of AMPK signaling clearly declines with aging. The loss of sensitivity of AMPK activation to cellular stress impairs metabolic regulation, increases oxidative stress and reduces autophagic clearance. These age-related changes activate innate immunity defence, triggering a low-grade inflammation and metabolic disorders. We will review in detail the signaling pathways of this integrated network through which AMPK controls energy metabolism, autophagic degradation and stress resistance and ultimately the aging process.

Subfields: Aging, Epidemiology, Geriatrics and Gerontology

View Paper: https://www.semanticscholar.org/paper/ca8cbeb4c0086a6ff926222b14fe4e90ca544c11

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Citations in the corpus

Context-Dependent and Disease-Specific Diversity in Protein Interactions within Stress Granules (2018, background): “, 2010), which also contains constitutive SG proteins (G3BP1, USP10, and CDC37) and may integrate aging and the cellular stress response (Salminen and Kaarniranta, 2012).”
Mitochondrial dysfunction in cell senescence and aging (2022, background): “The various mechanisms involved in Ca2+ overload–induced mitochondrial dysfunction include Ca2+-induced nitric oxide production; Ca2+-enhanced cytochrome c dissociation from the IMM; opening of the mitochondrial permeability transition pore (mPTP), which subsequently causes the release of cytochrome”
Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, neutral): “240,241 This is associated with decreased energy metabolism, oxidative stress, and in ﬂ ammation.”