Affiliation:
1. Laboratory of Molecular Biology of Exercise (LaBMEx), Faculty of Applied Sciences University of Campinas (UNICAMP) Limeira São Paulo Brazil
2. Department of Biology The University of Texas at Arlington (UTA) Arlington Texas USA
3. Laboratory of Nutritional Genomic, School of Applied Sciences University of Campinas (UNICAMP) Limeira São Paulo Brazil
4. Obesity and Comorbidities Research Center (OCRC) University of Campinas (UNICAMP) Campinas São Paulo Brazil
5. Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School University of São Paulo (USP) Ribeirão Preto São Paulo Brazil
Abstract
AbstractObesity is a worldwide multifactorial disease caused by an imbalance in energy metabolism, increasing adiposity, weight gain, and promoting related diseases such as diabetes, cardiovascular diseases, neurodegeneration, and cancer. Recent findings have reported that metabolic stress related to obesity induces a mitochondrial stress response called mitochondrial unfolded protein response (UPRmt), a quality control pathway that occurs in a nuclear DNA–mitochondria crosstalk, causing transduction of chaperones and proteases under stress conditions. The duality of UPRmt signaling, with both beneficial and detrimental effects, acts in different contexts depending on the tissue, cell type, and physiological states, affecting the mitochondrial function and efficiency and the metabolism homeostasis during obesity, which remains not fully clarified. Therefore, this review discusses the most recent findings regarding UPRmt signaling during obesity, bringing an overview of UPRmt across different metabolic tissues.
Funder
Fundação de Amparo à Pesquisa do Estado de São Paulo