Autophagy mediates the mitotic senescence transition

In the citing paper

“Some studies have touched on the functional relevance of autophagy in senescence, where its role appears to vary depending on cell type and senescence triggers (Patschan et al. 2007; Young et al. 2009; Leidal et al. 2012; Mosieniak et al. 2012; Singh et al. 2012; Dörr et al. 2013).”

In the citing paper

“In preclinical models, proteotoxic stress not only drives entry into a senescent state, but also activates autophagy, which consequently buffers toxicity from misfolded SASP factors 44,45 .”

In the citing paper

“they may have both similar and distinct functions that are tissue-or cell-type specific [637-641]”

In the citing paper

“The kinetics of these gene expression changes were similar to that of SASP components, implying some level of correlation between autophagy and the SASP.”

In the citing paper

“We recently showed that autophagy is activated during the dynamic phase of OIS in HDFs, which was accompanied by a concerted up-regulation of genes involved in both autophagy and lysosomal biogenesis (Young et al. 2009).”

In the citing paper

“Indeed, inhibition of autophagy suppressed the production of both IL6 and IL8 and delayed the establishment of senescence.”

In the citing paper

“ULK2 has a higher degree of identity with ULK1 than any of the other homologs”

In the citing paper

“macro-autophagy (hereafter referred to as autophagy)—a tightly regulated major lysosomal degradation pathway (27–30)—has been implicated in establishing the SASP through the target of rapamycin (TOR) autophagy spatial coupling compartment (TASCC).”

In the citing paper

“Our results indicate that autophagy is both a negative and a positive regulator of senescence, resolving apparently contradictory reports in the literature (31–33, 44).”

In the citing paper

“These cells use autophagy for their maintenance”

In the citing paper

“Autophagy is activated during senescence”

In the citing paper

“Autophagy is dynamically activated during OIS and facilitates the synthesis of interleukin 6 (IL-6) and IL-8, major components of the SASP 58,59 .”

In the citing paper

“and that the inhibition of autophagy delays of onset of senescence and SASP.”

In the citing paper

“Autophagy is also required for the execution of the senescence program because its inhibition delays the senescence-related cell cycle arrest and SASP factor accumulation, at least in OIS [244].”

In the citing paper

“In senescence induced by oncogenic Ras, protein synthesis and autophagic degradation are simultaneous activated, and the same cell displays high autophagic activity and activated mTOR, the autophagy inhibitor [244].”

In the citing paper

“Moreover, autophagy is required for some instances of cell-autonomous tumor suppression by senescence (e.g., in oncogene-induced senescence caused by HRAS V12 and BRAF V600E ) 156,157 and cell death (e.g., in the context of ferroptosis) 158 (Figure 3A).”

In the citing paper

“Of note, proficient autophagy is required for the successful establishment of OIS.156”

In the citing paper

“Although BNIP3L is typically thought of as pro-apoptotic [181], anti-apoptotic roles have been recently discovered, particularly in reactive astrocytes during ALS disease progression [35]. Similarly, BNIP3L has been shown to increase in senescent cells to direct mitochondria to autophagosomes for degradation [174].”