Alteration and role of heat shock proteins in acute pancreatitis.
Many etiological factors are involved in the pathogenesis of acute pancreatitis. The pathogenesis of acute pancreatitis has been attributed to such causes as trypsin autodigestion, pancreatic microcirculation malfunction, the calcium overload in pancreatic acinar cells, oxygen free radical injury, cytokine injury, and has been treated in detail in numerous reviews. More recently, heat shock proteins (HSP), particularly heat shock protein 60 (HSP60), have receive increasing attention as another possible factor in the pathogenesis and development of acute pancreatitis. This brief review aims to: (i) outline our current understanding of HSP and their role in pancreatitis; (ii) discuss the available evidences that suggest HSP's interplay between pancreas tissues and etiological agents; (iii) delineate the functional mechanisms of HSP proposed by different research groups, and offer new thinking in preventing and treating acute pancreatitis in general.
Feng
Jia Yan
JY
Department of Pathophysiology, Tongji University School of Medicine, Shanghai, China.
Li
Yong Yu
YY
D000208:Acute Disease; D017209:Apoptosis; D018834:Chaperonin 60 / Q000502:physiology; D055551:HSP27 Heat-Shock Proteins / Q000502:physiology; D018840:HSP70 Heat-Shock Proteins / Q000502:physiology; D006360:Heat-Shock Proteins / Q000737:chemistry / Q000502:physiology*; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D010195:Pancreatitis / Q000209:etiology*
D018834:Chaperonin 60; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D018836:Inflammation Mediators; D016328:NF-kappa B