Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Mitochondrial function and malfunction in the pathophysiology of pancreatitis

Gerasimenko, Oleg Vsevolodovich and Gerasimenko, Julia Vladimirovna 2012. Mitochondrial function and malfunction in the pathophysiology of pancreatitis. Pflugers Archiv European Journal of Physiology 464 (1) , pp. 89-99. 10.1007/s00424-012-1117-8

Full text not available from this repository.

Abstract

As a primary energy producer, mitochondria play a fundamental role in pancreatic exocrine physiology and pathology. The most frequent aetiology of acute pancreatitis is either gallstones or heavy alcohol consumption. Repeated episodes of acute pancreatitis can result in the development of chronic pancreatitis and increase the lifetime risk of pancreatic cancer 100-fold. Pancreatic cancer is one of the most common causes of cancer mortality with only about 3–4 % of patients surviving beyond 5 years. It has been shown that acute pancreatitis involves Ca2+ overload and overproduction of reactive oxygen species in pancreatic acinar cells. Both factors significantly affect mitochondria and lead to cell death. The pathogenesis of inflammation in acute and chronic pancreatitis is tightly linked to the induction of necrosis and apoptosis. There is currently no specific therapy for pancreatitis, but recent findings of an endogenous protective mechanism against Ca2+ overload—and particularly the potential to boost this protection—bring hope of new therapeutic approaches.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Subjects: R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Uncontrolled Keywords: Calcium; ATP; Pancreatic acinar cell
Publisher: Springer
ISSN: 0031-6768
Last Modified: 04 Jun 2017 04:05
URI: http://orca-mwe.cf.ac.uk/id/eprint/32581

Citation Data

Cited 15 times in Google Scholar. View in Google Scholar

Cited 17 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item