Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

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)...

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Main Authors: Enrique Gabandé-Rodríguez, Manuel M. Gómez de las Heras, María Mittelbrunn
Format: Article
Language:English
Published: MDPI AG 2019-12-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/9/1/82
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author Enrique Gabandé-Rodríguez
Manuel M. Gómez de las Heras
María Mittelbrunn
author_facet Enrique Gabandé-Rodríguez
Manuel M. Gómez de las Heras
María Mittelbrunn
author_sort Enrique Gabandé-Rodríguez
collection DOAJ
description 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<sup>+</sup> 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.
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spelling doaj.art-ab61b3e87c5d4f78a81667c14d2de8b82023-09-02T07:11:42ZengMDPI AGCells2073-44092019-12-01918210.3390/cells9010082cells9010082Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and MitochondriaEnrique Gabandé-Rodríguez0Manuel M. Gómez de las Heras1María Mittelbrunn2Immunometabolism 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, SpainImmunometabolism 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, SpainImmunometabolism 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, SpainMitochondrial 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<sup>+</sup> 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.https://www.mdpi.com/2073-4409/9/1/82autophagymitochondriacalorie restrictionagingmetabolisminflammation
spellingShingle Enrique Gabandé-Rodríguez
Manuel M. Gómez de las Heras
María Mittelbrunn
Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria
Cells
autophagy
mitochondria
calorie restriction
aging
metabolism
inflammation
title Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria
title_full Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria
title_fullStr Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria
title_full_unstemmed Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria
title_short Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria
title_sort control of inflammation by calorie restriction mimetics on the crossroad of autophagy and mitochondria
topic autophagy
mitochondria
calorie restriction
aging
metabolism
inflammation
url https://www.mdpi.com/2073-4409/9/1/82
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AT manuelmgomezdelasheras controlofinflammationbycalorierestrictionmimeticsonthecrossroadofautophagyandmitochondria
AT mariamittelbrunn controlofinflammationbycalorierestrictionmimeticsonthecrossroadofautophagyandmitochondria