Open Access

REVIEW

Role of RIPK1 in the pathogenesis of acute respiratory distress syndrome

XUNAN ZHAO^#, EMMANUEL MAGO^#, DAN WENG^*

School of Environmental and Biological Engineering, Nanjing University of Science & Technology, Nanjing, China

* Corresponding Author: DAN WENG. Email:

BIOCELL 2023, 47(10), 2151-2162. https://doi.org/10.32604/biocell.2023.030570

Received 13 April 2023; Accepted 26 July 2023; Issue published 08 November 2023

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening pulmonary disease typically caused by microbial infections, trauma, inhalation of harmful gases, and other factors. It is characterized by an inflammation in the lungs and increased alveolar permeability, leading to pulmonary edema and consequently, a low oxygen supply or hypoxemia. ARDS is responsible for 1 in 10 admissions to intensive care units, and the mortality rate for patients with severe ARDS is as high as 46%. Extensive efforts have been devoted to investigating the pathological mechanisms of ARDS to develop new effective clinical strategies. Recent studies have reported that receptor-interacting serine/threonine kinase 1 (RIPK1) is involved in the pathogenesis of ARDS. RIPK1 is a critical mediator of programmed cell death and inflammation. Growing evidence suggests that RIPK1 plays a role in the pathogenesis of different inflammatory diseases and serves as a promising pharmaceutical target. This review summarizes and sheds some light on the recent findings regarding the role of RIPK1 and related molecules in the pathogenesis of ARDS.

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