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In acinar cells, cellular organelles like zymogene granule, mitochondria, endoplasmic reticulum and lysosome functions in coordinate way in order to synthesize and secrets large amounts of digestive enzyme. Dysfunction of this organelle, results into enzyme activation within acinar cell; ultimately, acute pancreatitis. While previous studies reported that mitochondrial function is disrupt but mechanism of clearance of these mitochondria remains unknown during pancreatitis. Here we reported that PINK1 and Parkin mediated pathway is activated during pancreatitis and clears dysfunctional mitochondria in-vivo. PINK1 or Parkin deficient acinar cell had energy crisis, decreased ATP production and altered acinar cell fate in-vitro. Inhibiting clearance of dysfunctional mitochondria aggravates experimental pancreatitis severity and delays regeneration/recovery of exocrine tissue after disease via PARIS-PGC-1α pathway. While an attempt to explore therapeutic target of PARIS-PGC-1α pathway by treatment of SRT1720 rescued experimental pancreatitis. Together, PINK1 and Parkin, restricts exocrine pancreatic damage in pancreatitis and accelerates tissue recovery after disease.