University of Tasmania
Browse

File(s) under permanent embargo

Autophagy, a process within reperfusion injury: an update

journal contribution
posted on 2023-05-21, 02:28 authored by Thapalia, BA, Zhen ZhouZhen Zhou, Lin, X
Autophagy is an important constitutive intracellular catalytic process that occurs in basal conditions, as well as during stress in all tissues. It is induced during cellular growth, tissue differentiation and metabolic demands. The regulated expression is cytoprotective while its deregulation leads to varieties of diseases. It plays a vital role in ischemic heart disease, being beneficial and adaptive during ischemia while detrimental and lethal during reperfusion. Reperfusion injury is the consequence of this deregulated autophagy and the motive of its persistence during reperfusion is still obscure. A long standing debate persists as to the dual nature of autophagy and defining its clearer role in cell death as compared to the widely studied process, apoptosis. Despite the progresses in understanding of the process and identification of critical mediators, there is no therapeutic strategy to address its final outcome, the reperfusion injury. This lack of effective therapeutic strategies has even questioned the validity of the process as a single entity. We still continue to witness the devastation with standard cure of reperfusion. In this article, we review the process, highlight reperfusion injury and outline important studies being conducted for the prevention of reperfusion injury and offer cardio-protection.

History

Publication title

International Journal of Clinical and Experimental Pathology

Volume

7

Issue

12

Pagination

8322-8341

ISSN

1936-2625

Department/School

Menzies Institute for Medical Research

Publisher

e-Century Pub. Corp.

Place of publication

United States

Rights statement

Copyright 2014 IJCEP

Repository Status

  • Restricted

Socio-economic Objectives

Other health not elsewhere classified

Usage metrics

    University Of Tasmania

    Categories

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC