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Mol. Cells 2010; 29(4): 327-332

Published online March 31, 2010

https://doi.org/10.1007/s10059-010-0066-3

© The Korean Society for Molecular and Cellular Biology

Physiological Consequences of Programmed Necrosis, an Alternative form of Cell Demise

Young Sik Cho*, Seung Yeon Park, Hee Suk Shin, and Francis Ka-Ming Chan1

Pharmacology Research Center, Bio-organic Science Division, Korea Research Institute of Chemical Technology, Daejeon 305-600, Korea, 1Depart-ment of Pathology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA

Correspondence to : *Correspondence: yscho@krict.re.kr

Received: February 19, 2010; Accepted: February 22, 2010

Abstract

Cell death occurs spontaneously or in response to exter-nal stimuli, and can be largely subdivided into apoptosis and necrosis by the distinct morphological and biochemical features. Unlike apoptosis, necrosis was recognized as the passive and unwanted cell demise committed in a nonregulated and disorganized manner. However, under specific conditions such as caspase intervention, necrosis has been proposed to be regulated in a well-orchestrated way as a backup mechanism of apoptosis. The term programmed necrosis has been coined to describe such an alternative cell death. Recently, at least some regulators governing programmed necrosis have been identified and demonstrated to be interconnected via a wide network of signal pathways by further extensive studies. There is growing evidence that programmed necrosis is not only associated with pathophysiological diseases, but also provides innate immune response to viral infection. Here, we will introduce recent updates on the molecular me-chanism and physiological significance of programmed necrosis.

Keywords apoptosis, inflammation, programmed necrosis, receptor interacting protein, TNFα

Article

Minireview

Mol. Cells 2010; 29(4): 327-332

Published online March 31, 2010 https://doi.org/10.1007/s10059-010-0066-3

Copyright © The Korean Society for Molecular and Cellular Biology.

Physiological Consequences of Programmed Necrosis, an Alternative form of Cell Demise

Young Sik Cho*, Seung Yeon Park, Hee Suk Shin, and Francis Ka-Ming Chan1

Pharmacology Research Center, Bio-organic Science Division, Korea Research Institute of Chemical Technology, Daejeon 305-600, Korea, 1Depart-ment of Pathology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA

Correspondence to:*Correspondence: yscho@krict.re.kr

Received: February 19, 2010; Accepted: February 22, 2010

Abstract

Cell death occurs spontaneously or in response to exter-nal stimuli, and can be largely subdivided into apoptosis and necrosis by the distinct morphological and biochemical features. Unlike apoptosis, necrosis was recognized as the passive and unwanted cell demise committed in a nonregulated and disorganized manner. However, under specific conditions such as caspase intervention, necrosis has been proposed to be regulated in a well-orchestrated way as a backup mechanism of apoptosis. The term programmed necrosis has been coined to describe such an alternative cell death. Recently, at least some regulators governing programmed necrosis have been identified and demonstrated to be interconnected via a wide network of signal pathways by further extensive studies. There is growing evidence that programmed necrosis is not only associated with pathophysiological diseases, but also provides innate immune response to viral infection. Here, we will introduce recent updates on the molecular me-chanism and physiological significance of programmed necrosis.

Keywords: apoptosis, inflammation, programmed necrosis, receptor interacting protein, TNFα

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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