RESUMO
Chronic inflammation impairs skeletal muscle regeneration. Although many cells are involved in chronic inflammation, macrophages seem to play an important role in impaired muscle regeneration since these cells are associated with skeletal muscle stem cell (namely, satellite cells) activation and fibro-adipogenic progenitor cell (FAP) survival. Specifically, an imbalance of M1 and M2 macrophages seems to lead to impaired satellite cell activation, and these are the main cells that function during skeletal muscle regeneration, after muscle damage. Additionally, this imbalance leads to the accumulation of FAPs in skeletal muscle, with aberrant production of pro-fibrotic factors (e.g., extracellular matrix components), impairing the niche for proper satellite cell activation and differentiation. Treatments aiming to block the inflammatory pro-fibrotic response are partially effective due to their side effects. Therefore, strategies reverting chronic inflammation into a pro-regenerative pattern are required. In this review, we first describe skeletal muscle resident macrophage ontogeny and homeostasis, and explain how macrophages are replenished after muscle injury. We next discuss the potential role of chronic physical activity and exercise in restoring the M1 and M2 macrophage balance and consequently, the satellite cell niche to improve skeletal muscle regeneration after injury.
Assuntos
Exercício Físico , Desenvolvimento Muscular/genética , Músculo Esquelético/crescimento & desenvolvimento , Células Satélites de Músculo Esquelético/citologia , Adipogenia/genética , Diferenciação Celular/genética , Humanos , Inflamação/genética , Inflamação/patologia , Inflamação/terapia , Macrófagos/metabolismo , Músculo Esquelético/lesões , Regeneração/genética , Células Satélites de Músculo Esquelético/metabolismo , Nicho de Células-Tronco/genéticaRESUMO
A obesidade está intimamente ligada ao estado inflamatório, sendo considerada uma patologia metabólica complexa. Dietas hipercalóricas alteram a composição da microbiota intestinal, sendo a mudança da proporção de bactérias dos filos Bacteroidetes e Firmicutes uma das consequências mais conhecidas. Essa mudança determina a produção de metabólitos específicos do sistema imune, induzindo estado inflamatório responsável pelo agravamento de uma série de doenças. A dieta hipercalórica representa um fator de risco para a obesidade e para o diabetes mellitus, doenças interligadas pelo conceito de lipotoxicidade, e o estado inflamatório também contribui para o aparecimento e para a progressão de doenças cardiovasculares. Com esse artigo, objetivamos estudar a obesidade pela perspectiva imunológica e microbiológica, abordando as consequências de dietas hipercalóricas sobre o estado inflamatório e a sobre a microbiota. Ademais, associar a mudança no microbioma a doenças prevalentes como o diabetes mellitus e as doenças cardiovasculares, apontando abordagens terapêuticas potenciais.
Obesity is closely linked to an inflammatory state, being considered a complex metabolic pathology. Hypercaloric diets alter the composition of intestinal microbiota, and the change in the proportion of bacteria from the Bacteroidetes and Firmicutes phyla is one of the most known consequences. This change causes the production of specific immune system metabolites, inducing an inflammatory state which is responsible for aggravating some diseases. The hypercaloric diet represents a risk factor for obesity and diabetes mellitus, diseases linked by the concept of lipotoxicity, and the inflammatory state also contributes to the onset and to the progression of cardiovascular diseases. In this article, we aim to study obesity from the immunological and microbiological perspective, addressing the consequences of hypercaloric diets on the inflammatory state and microbiota. In addition, to analyze the role of microbiome change in prevalent diseases like diabetes mellitus and cardiovascular diseases, pointing out potential therapeutic approaches.