biostudies-literatureLin HHNIDCR NIH HHSNHLBI NIH HHSe1478https://www.ebi.ac.uk/biostudies/studies/S-EPMC4649523biostudies-literatureUnknown5Autophagy maintains cell and tissue homeostasis through catabolic degradation. To better delineate the in vivo function for autophagy in adaptive responses to tissue injury, we examined the impact of compromised autophagy in mouse submandibular glands (SMGs) subjected to main excretory duct ligation. Blocking outflow from exocrine glands causes glandular atrophy by increased ductal pressure. Atg5(f/-);Aqp5-Cre mice with salivary acinar-specific knockout (KO) of autophagy essential gene Atg5 were generated. While duct ligation induced autophagy and the expression of inflammatory mediators, SMGs in Atg5(f/-);Aqp5-Cre mice, before ligation, already expressed higher levels of proinflammatory cytokine and Cdkn1a/p21 messages. Extended ligation period resulted in the caspase-3 activation and aciCell death & diseaseDynamic involvement of ATG5 in cellular stress responses.PMC4649523R01DE14183R01 HL112638R01 DE010742R01DE10742R01 DE014183RC1 DE020335RC1DE020335Mizushima NLin SMBorok ZLin HHVonderfecht SLimesand KHCamden JMAnn DKFlodby PChung YfalseDynamic involvement of ATG5 in cellular stress responses.Autophagy maintains cell and tissue homeostasis through catabolic degradation. To better delineate the in vivo function for autophagy in adaptive responses to tissue injury, we examined the impact of compromised autophagy in mouse submandibular glands (SMGs) subjected to main excretory duct ligation. Blocking outflow from exocrine glands causes glandular atrophy by increased ductal pressure. Atg5(f/-);Aqp5-Cre mice with salivary acinar-specific knockout (KO) of autophagy essential gene Atg5 were generated. While duct ligation induced autophagy and the expression of inflammatory mediators, SMGs in Atg5(f/-);Aqp5-Cre mice, before ligation, already expressed higher levels of proinflammatory cytokine and Cdkn1a/p21 messages. Extended ligation period resulted in the caspase-3 activation and aci2014-01-01T00:00:00Z2014 Oct2025-05-29T22:28:14.056Z2025-05-29T22:28:14.056ZS-EPMC46495232534103210.1038/cddis.2014.428