2026-04-13T07:29:17Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1717282025-12-04T19:01:55Zcom_2072_1057col_2072_478777col_2072_478917

00925njm 22002777a 4500 dc Tur Torres, Juan author Pereira Lopes, Selma Patrícia author Vico Rivero, Tania author Marín, Eros A. author Muñoz, Juan Pablo author Hernández-Alvarez, María Isabel author Cardona, Pere-Joan author Zorzano Olarte, Antonio author Lloberas Cavero, Jorge author Celada Cotarelo, Antonio author 2020-11-03T09:56:23Z 2020-11-03T09:56:23Z 2020-09-25 2020-11-03T09:56:23Z Mitofusin 2 (Mfn2) plays a major role in mitochondrial fusion and in the maintenance of mitochondria-endoplasmic reticulum contact sites. Given that macrophages play a major role in inflammation, we studied the contribution of Mfn2 to the activity of these cells. Pro-inflammatory stimuli such as lipopolysaccharide (LPS) induced Mfn2 expression. The use of the Mfn2 and Mfn1 myeloid-conditional knockout (KO) mouse models reveals that Mfn2 but not Mfn1 is required for the adaptation of mitochondrial respiration to stress conditions and for the production of reactive oxygen species (ROS) upon pro-inflammatory activation. Mfn2 deficiency specifically impairs the production of pro-inflammatory cytokines and nitric oxide. In addition, the lack of Mfn2 but not Mfn1 is associated with dysfunctional autophagy, apoptosis, phagocytosis, and antigen processing. Mfn2floxed;CreLysM mice fail to be protected from Listeria, Mycobacterium tuberculosis, or LPS endotoxemia. These results reveal an unexpected contribution of Mfn2 to ROS production and inflammation in macrophages. Mitocondris Autofàgia Respiració Apoptosi Homeòstasi Mitochondria Autophagy Respiration Apoptosis Homeostasis Mitofusin 2 in macrophages links mitochondrial ROS production, cytokine release, phagocytosis, autophagy, and bactericidal activity