Autophagy and aging.

By D. Rubinsztein, Guillermo Mariño, Guido Kroemer. Cell, 2011

2,083 citations recorded by the source corpus.

Subfields: Epidemiology, Geriatrics and Gerontology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/497b0d3302555dce0c717607e8744951009b8bc7

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Citations in the corpus

Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms (2017, background): “Autophagy is necessary for cellular viability[496_TD$DIFF], and autophagic dysfunction has been linked to neurodegeneration, aging, and age-related diseases [18].”
Autophagy: Renovation of Cells and Tissues (2011, background): “Interestingly, many regimes that promote longevity, including calorie restriction, TOR suppression, sirtuin activation, and spermidine treatment, are able to induce autophagy (Madeo et al., 2010; Rubinsztein et al., 2011).”
Protein Misfolding, Amyloid Formation, and Human Disease: A Summary of Progress Over the Last Decade. (2017, background): “In addition, both macroautophagy and chaperone-mediated autophagy decrease their efficiency as a result of the transcriptional downregulation of autophagy-related proteins and decreased levels of lysosomal membrane receptors, respectively (226).”
TFEB-mediated autophagy rescues midbrain dopamine neurons from α-synuclein toxicity (2013, methodology): “The transfection into HEK 293 cells was carried out using the calcium-phosphate method, and included the packaging plasmids pDP6 encoding AAV6 capsid proteins (3, 4).”
The hallmarks of aging. (2013, background): “…proteolytic systems implicated in protein quality control—namely, the autophagy-lysosomal system and the ubiquitin-proteasome system—decline with aging (Rubinsztein et al., 2011; Tomaru et al., 2012), supporting the idea that collapsing proteostasis constitutes a common feature of old age.”
Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “The efficiency of the lysosome in degrading cellular components has been shown to decline over time, an effect that has been linked to the development of aging and age-related diseases, such as neurodegeneration and cancer (reviewed by Rubinsztein et al., 2011).”
Measuring in vivo mitophagy (2015, background): “There ular Cell 60, 685–696, November 19, 2015 ª2015 Elsevier Inc. 693 is particular interest in the role of autophagy and more specifically mitophagy as a contributor to neurodegenerative disease, and to aging itself (Madeo et al., 2015; Rubinsztein et al., 2011; Wong and Cuervo, 2010).”
Links between metabolism and cancer. (2012, background): “Inhibition of autophagy enhances senescence, which could be related to the inability of cells to clear defective mitochondria, thereby increasing oxidative stress and aging (Rabinowitz and White 2010; Rubinsztein et al. 2011).”
Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “263,264 Although autophagy can be either tumor-suppressive or tumor-promoting, depending on the context, the precise mechanisms that determine the role of autophagy are not well-de ﬁ ned.”
Phosphorylation of p62 activates the Keap1-Nrf2 pathway during selective autophagy. (2013, background): “…in the M oxidative-stress response, metabolic pathways, and innate immunity, and dysregulation of these processes is associated with pathogenic mechanisms of multiple human diseases, including tumor development (Kensler et al., 2007; Rubinsztein et al., 2011; Sporn and Liby, 2012; White, 2012).”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “Thus, a decline in autophagy efficiency during aging (Rubinsztein et al., 2011; Taylor and Dillin, 2011) leads to”