Chinese Journal of Physiology

REVIEW ARTICLE
Year
: 2019  |  Volume : 62  |  Issue : 2  |  Page : 53--62

Autophagy: A potential target for rescuing sepsis-induced hepatic failure


Chin Hsu 
 Department of Physiology, Faculty of Medicine, College of Medicine, Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan

Correspondence Address:
Prof. Chin Hsu
Department of Physiology, Faculty of Medicine, College of Medicine, Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung
Taiwan

Sepsis is the leading cause of death in intensive care units worldwide; however, it remains a scientific and clinical challenge in modern medicine. An excessive inflammatory response associated with high level of reactive oxygen species results in mitochondrial dysfunction and activation of the unfolded protein response leading to subsequent energetic organ failure in septic patients. In addition to blocking the inflammatory cascade directly, new strategies focusing on host endogenous adaption to severe infection may hold better promise for improving outcomes in septic patients. Autophagy is a fundamental cellular response to stress and pathogen invasion. The study of autophagic responses to sepsis is a critical component of understanding the mechanisms by which tissues respond to infection. This review aims at elucidating the role of autophagy in sepsis-induced hepatic failure and further explores the possible factor that suppresses autophagy and potential targets of augmenting autophagy, in an effort to provide a new perspective for the clinical treatment of sepsis-induced hepatic failure.


How to cite this article:
Hsu C. Autophagy: A potential target for rescuing sepsis-induced hepatic failure.Chin J Physiol 2019;62:53-62


How to cite this URL:
Hsu C. Autophagy: A potential target for rescuing sepsis-induced hepatic failure. Chin J Physiol [serial online] 2019 [cited 2020 Oct 22 ];62:53-62
Available from: https://www.cjphysiology.org/article.asp?issn=0304-4920;year=2019;volume=62;issue=2;spage=53;epage=62;aulast=Hsu;type=0