Autophagy (https://en.wikipedia.org/wiki/Autophagy)
Fasting activates Autophagy – Caloric restriction affects 5 molecular pathways that activate autophagy
Sunlight, Vitamin D3 and Klotho activate Autophagy – there are three waysthrough which UV light, Vitamin D, and the Klotho activate autophagy viainhibiting the Insulin/ Insulin-like growth factor 1 (IGF-1) pathway.
Rapamycin activates Autophagy – there are two ways through which mTOR inhibitors activate autophagy – TORC1 and TORC2 mechanisms
Caffeine activates Autophagy – Caffeine can activate autophagy via anmTOR-dependent mechanism
Green tea activates Autophagy – ECGC can activate autophagy via anmTOR-dependent mechanism
Metformin activates Autophagy – metformin can activate autophagy via AMP-activated protein kinase (AMPK) activation – mTOR-dependent andmTOR-independent mechanisms
Lithium activates Autophagy – lithium and other compounds can activate autophagy by inhibiting inositol monophosphate and lower IP3 levels – anmTOR-independent mechanism
Reservatrol activates Autophagy – there are four 4 ways through whichresveratrol can activate autophagy – via mTOR-dependent and mTOR-independent mechanisms
Spermidine activates Autophagy – how spermidine activates autophagy viahistone protein deacetylation – mTOR-indepdendent mechanism
Hypoxia sctivates Autophagy – intermittent hypoxia can increase autophagyvia HIF-1a
Phytosubstances which activate the Nrf2 pathway can activate Autophagy. These are many and include soy products and Hot peppers.
*In addition, these lesser-known substances can also activate autophagy:
Amiodarone low dose Cytoplasm – midstream yes Calcium channel blocker => TORC1 inhibition. Also, a mTOR-independent autophagy inducer
Fluspirilene low dose Cytoplasm – midstream yes Dopamine antagnoists => mTOR-dependent autophagy induction
Penitrem A low dose Cytoplasm – midstream yes high conductance Ca++activated K+ channel inhibitor => mTOR-dependent autophagy inducer
Perihexilene low dose Cytoplasm- midstream yes 1. TORC1 inhibition
Niclosamide low dose Cytoplasm- midstream yes 1. TORC1 inhibition
Trehalose 100 mM Cytoplasm – midstream supplement 1. activates autophagy via an mTOR-independent mechanism
Torin-1 low dose Cytoplasm – midstream no 1. mTOR inhibition (muchmore potent than rapamycin)
Trifluoperazine low dose Cytoplasm – midstream yes Dopamineantagonists => mTOR-dependent autophagy induction
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Autophagy is like having a Pac man inside each of your cells, chasing down, eating up and recycling dysfunctional organelles, proteins andprotein aggregates. It has three forms: i. chaperone-mediated autophagy, ii. microautophagy and iii. macroautophagy. The last is the most importantone.
Autophagy is a stress response and behaves according to the principles of hormesis.
Autophagy can retire and eat up old Mitochondria which have become electron-leaking engines.
Autophagy solves the problem of high baseline levels of reactive oxygen and nitrogen species.
Autophagy does not require proteins to be unfolded for it to work and therefore can perform housekeeping tasks undoable by the other cell-level house cleaning system, the ubiquitin-proteasome system.
Autophagy gets rid of the protein aggregates that can make you lose your memory and/or walk slow as you grow old – those associated with Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, ALS, CTE, and other Neurodegenerative disease.
Autophagy keeps adult stem cells healthy and facilitates their capability to differentiate to make normal somatic body cells.
Autophagy prevents Inflammation – it works hand-in-hand with apoptosis to help the body get rid of dying cells without inducing cell rupture and inflammation.
Autophagy prevents cancer – it helps maintain genetic stability, prevents epigenetic gene silencing. And it helps promote Oncogene-induced cellular Senescence for cancer prevention.
Autophagy saves the lives of cells by preventing unnecessary cellular Apoptosis and cellular Necrosis.
Autophagy is involved in Nrf2 activation and to some extent Nrf2 expression negatively regulates autophagy.
Autophagy keeps your Bone marrow stem cell population alive and functional.
Autophagy helps with infections – it helps clear intracellular pathogenssuch as Bacteria and Viruses.
Autophagy improves the innate immune response.
We are starting to understand why autophagy declines with aging.
While autophagy declines with aging, it can exercise multiple effects to slow aging down. It inhibits the major mechanisms of aging such as cellular senescence, protein aggregate build-up, stem cell loss, epigenetic gene silencing, Telomere shortening, and oxidative damage to proteins, lipids and DNA.
There are many practical ways to activate Autophagy like consuming green tea and caffeine and some less-practical ones.
IN: www.anti-agingfirewalls.com/…/autophagy-the-housekeeper-in-… (#16. Practical interventions to promote autophagy)
Akira Morikawa 