| Autor: |
Gabandé-Rodríguez E; Immunometabolism and Inflammation Laboratory, Tissue and Organ homeostasis Program, Cell-Cell Communication and Inflammation Unit, Centro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (UAM), 28049 Madrid, Spain.; Department of Molecular Biology, Faculty of Sciences, Universidad Autónoma de Madrid (UAM), 28049 Madrid, Spain.; Regulation of Cellular Homeostasis Laboratory, Area of Rare and Genetically Based Diseases, Instituto de Investigación Hospital 12 de Octubre, 28041 Madrid, Spain., Gómez de Las Heras MM; Immunometabolism and Inflammation Laboratory, Tissue and Organ homeostasis Program, Cell-Cell Communication and Inflammation Unit, Centro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (UAM), 28049 Madrid, Spain.; Department of Molecular Biology, Faculty of Sciences, Universidad Autónoma de Madrid (UAM), 28049 Madrid, Spain.; Regulation of Cellular Homeostasis Laboratory, Area of Rare and Genetically Based Diseases, Instituto de Investigación Hospital 12 de Octubre, 28041 Madrid, Spain., Mittelbrunn M; Immunometabolism and Inflammation Laboratory, Tissue and Organ homeostasis Program, Cell-Cell Communication and Inflammation Unit, Centro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (UAM), 28049 Madrid, Spain.; Department of Molecular Biology, Faculty of Sciences, Universidad Autónoma de Madrid (UAM), 28049 Madrid, Spain.; Regulation of Cellular Homeostasis Laboratory, Area of Rare and Genetically Based Diseases, Instituto de Investigación Hospital 12 de Octubre, 28041 Madrid, Spain. |
| Abstrakt: |
Mitochondrial metabolism and autophagy are two of the most metabolically active cellular processes, playing a crucial role in regulating organism longevity. In fact, both mitochondrial dysfunction or autophagy decline compromise cellular homeostasis and induce inflammation. Calorie restriction (CR) is the oldest strategy known to promote healthspan, and a plethora of CR mimetics have been used to emulate its beneficial effects. Herein, we discuss how CR and CR mimetics, by modulating mitochondrial metabolism or autophagic flux, prevent inflammatory processes, protect the intestinal barrier function, and dampen both inflammaging and neuroinflammation. We outline the effects of some compounds classically known as modulators of autophagy and mitochondrial function, such as NAD + precursors, metformin, spermidine, rapamycin, and resveratrol, on the control of the inflammatory cascade and how these anti-inflammatory properties could be involved in their ability to increase resilience to age-associated diseases. |
