Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Ahangari, F; Price, NL; Malik, S; Chioccioli, M; Barnthaler, T; Adams, TS; Kim, J; Pradeep, SP; Ding, SZ; Cosmos, CC; Rose, KAS; McDonough, JE; Aurelien, NR; Ibarra, G; Omote, N; Schupp, JC; DeIuliis, G; Nunez, JAV; Sharma, L; Ryu, C; Cruz, CSD; Liu, XR; Prasse, A; Rosas, I; Bahal, R; Fernandez-Hernando, C; Kaminski, N.
microRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis
JCI INSIGHT. 2023; 8(4): e158100 Doi: 10.1172/jci.insight.158100 [OPEN ACCESS]
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Co-Autor*innen der Med Uni Graz
Bärnthaler Thomas

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Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal disease. Recent findings have shown a marked metabolic reprogramming associated with changes in mitochondrial homeostasis and autophagy during pulmonary fibrosis. The microRNA-33 (miR-33) family of microRNAs (miRNAs) encoded within the introns of sterol regulatory element binding protein (SREBP) genes are master regulators of sterol and fatty acid (FA) metabolism. miR-33 controls macrophage immunometabolic response and enhances mitochondrial biogenesis, FA oxidation, and cholesterol efflux. Here, we show that miR-33 levels are increased in bronchoalveolar lavage (BAL) cells isolated from patients with IPF compared with healthy controls. We demonstrate that specific genetic ablation of miR-33 in macrophages protects against bleomycin-induced pulmonary fibrosis. The absence of miR-33 in macrophages improves mitochondrial homeostasis nucleic acids (PNA-33) attenuates fibrosis in different in vivo and ex vivo mice and human models of pulmonary fibrosis. These studies elucidate a major role of miR-33 in macrophages in the regulation of pulmonary fibrosis and uncover a potentially novel therapeutic approach to treat this disease.

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