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Fushimi, K., Nakashima, S., Banno, Y., et al. (2004) Implication of Prostaglandin E(2) in TNF-alpha-Induced Release of m-Calpain from HCS-2/8 Chondrocytes. Inhibition of m-Calpain Release by NSAIDs. Osteoarthritis and Cartilage, 12, 895-903.
https://doi.org/10.1016/j.joca.2004.08.001

has been cited by the following article:

• TITLE: Calpain-1 Mediated Mitochondria ROS/NLRP3 Inflammasome in Atherosclerosis

  AUTHORS: Futian Tang, Mohamed Ali Awad

  KEYWORDS: Calpain-1, ROS/NLRP3 Inflammasome, Atherosclerosis (AS)

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.11 No.4, April 12, 2023

  ABSTRACT: Calpains are calcium-activated cysteine proteases. There are two main isoforms of calpain that are ubiquitously expressed in tissues, calpain μ or calpain 1, which requires micromolar Ca2+ for activation, and calpain or 2, which requires millimolar Ca2+ for activation. The presence of other calpains is tissue specific. Atherosclerosis (AS) is an important risk factor for cerebral infarction, coronary heart disease and peripheral vascular disease. It was originally thought that AS was caused by impaired lipid metabolism. This research briefly reviewed Calpain Family, the structure and activation mechanism of calpain1, Calpains in the pathogenesis of atherosclerosis, NLRP3 structural characteristics and activation, ROS/NLRP3 inflammasome activation mechanism and ROS/NLRP3 inflammasome in atherosclerosis. The research showed that the Calpain-1 may play an important role in mitochondrial ROS/NLRP3 inflammasome in atherosclerosis.