PMC:7565665 / 15859-17432 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7565665","sourcedb":"PMC","sourceid":"7565665","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7565665","text":"Despite the importance of autophagy, there are many conditions where this process can become dysfunctional, leading to various pathological states. In the lungs, the major sources of autophagy dysfunction includes first- and second-hand cigarette smoke (CS) exposure and aging [35,62,93]. Studies have demonstrated that CS exposure can decrease the expression of transcription factor-EB (TFEB), a master autophagy regulator [34,35]. This occurs by the dysfunctional processing of TFEB in response to CS, causing the perinuclear localization of TFEB which prevents the activation of autophagy [62]. This CS-induced autophagy impairment of TFEB leads to impaired bacterial clearance [22,33,34,35]. Furthermore, there is evidence that CS exposure increases the accumulation of ubiquitinated proteins and p62 (a marker of autophagy impairment) in aggresome bodies, further impairing autophagy [22,34]. These deleterious effects of CS exposure on autophagy have also been demonstrated to be present in eCV exposure, which similarly impairs autophagy through the accumulation of aggresome bodies [39,94]. Furthermore, increasing the severity of pulmonary dysfunction and autophagy impairment has been observed to statistically correlate directly with increased levels of aggresome bodies [36], demonstrating its potential as a prognostic biomarker. Hence, CS exposure demonstrates a common, but preventable way autophagy can be impaired in individuals. Notably, CS exposure accelerates lung aging, known to be initiated by autophagy decline, which can exacerbate infections 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