<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Charmpilas, N.</style></author><author><style face="normal" font="default" size="100%">Fang, E. F.</style></author><author><style face="normal" font="default" size="100%">Palikaras, K.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mitophagy and neuroinflammation: a compelling interplay</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Neuropharmacol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Ageing</style></keyword><keyword><style  face="normal" font="default" size="100%">Energy homeostasis</style></keyword><keyword><style  face="normal" font="default" size="100%">immunity</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondria</style></keyword><keyword><style  face="normal" font="default" size="100%">mitophagy</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurodegeneration</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2022</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jun 28</style></date></pub-dates></dates><edition><style face="normal" font="default" size="100%">2022/06/29</style></edition><isbn><style face="normal" font="default" size="100%">1875-6190 (Electronic)1570-159X (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Mitochondria are the main sites of energy production and a major source of metabolic stress. Not surprisingly, impairment of mitochondrial homeostasis is tightly associated with the development and progression of a broad spectrum of human pathologies, including neurodegenerative disorders. Mitophagy mediates the selective degradation of damaged organelles, thus promoting cellular viability and tissue integrity. Defective mitophagy triggers cellular senescence and prolonged neuroinflammation, leading eventually to cell death and brain homeostasis collapse. Here, we survey the intricate interplay between mitophagy and neuroinflammation, highlighting that mitophagy can be a focal point for therapeutic interventions to tackle neurodegeneration.</style></abstract><accession-num><style face="normal" font="default" size="100%">35762540</style></accession-num><notes><style face="normal" font="default" size="100%">Charmpilas, NikolaosFang, Evandro FeiPalikaras, KonstantinosengUnited Arab EmiratesCurr Neuropharmacol. 2022 Jun 28. pii: CN-EPUB-124857. doi: 10.2174/1570159X20666220628153632.</style></notes><auth-address><style face="normal" font="default" size="100%">Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lorenskog, Norway.The Norwegian Centre on Healthy Ageing (NO-Age), Oslo, Norway.Department of Physiology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.</style></auth-address></record></records></xml>