Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function

Lima, Natália da Silva; Fondevila, Marcos F.; Novoa, Eva María; Buqué, Xabier; Mercado-Gómez, María; Gallet, Sarah; Gonzalez-Rellan, María J.; Fernandez, Uxia; Loyens, Anne; García-Vence, Maria; Chantada-Vázquez, María Del Pilar; Bravo, Susana B.; Marañón, Patricia; Senra, Ana; Escudero, Adriana; Leiva, Magdalena; Guallar, Diana; Fidalgo, Miguel; Gomes, Pedro; Claret, Marc; Sabio, Guadalupe; Varela‐Rey, Marta; Delgado, Teresa C.; Montero‐Vallejo, Rocío; Ampuero, Javier; López, Miguel; Diéguez, Carlos; Herrero, Laura; Serra, Dolors; Schwaninger, Markus; Prévot, Vincent; Gallego‐Durán, Rocío; Romero–Gómez, Manuel; Iruzubieta, Paula; Crespo, Javier; Martínez‐Chantar, María Luz; García‐Monzón, Carmelo; González-Rodrı́guez, Águeda; Aspichueta, Patricia; Nogueiras, Rubén

doi:10.1016/j.jhep.2021.09.008

Cited by 23 publications

(20 citation statements)

References 40 publications

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“…However, recent study by Lima et al reports that unlike mice autophagic activity may be associated in progression of hepatic steatosis in humans. Knockdown of ATG3 in human hepatocyte ameliorated hepatic steatosis condition while overexpression of ATG3 increased lipid load in hepatocytes ( 89 ). This renders possibility that autophagic model may function differently depending on the organism.…”

Section: Sirt1-mediated Autophagy and Endocrine Disordersmentioning

confidence: 99%

SIRT1 and Autophagy: Implications in Endocrine Disorders

et al. 2022

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Autophagy is a cellular process involved in the selective degradation and recycling of dysfunctional intracellular components. It plays a crucial role in maintaining cellular homeostasis and survival by removing damaged and harmful proteins, lipids, and organelles. SIRT1, an NAD+-dependent multifunctional enzyme, is a key regulator of the autophagy process. Through its deacetylase activity, SIRT1 participates in the regulation of different steps of autophagy, from initiation to degradation. The levels and function of SIRT1 are also regulated by the autophagy process. Dysregulation in SIRT1-mediated autophagy hinders the proper functioning of the endocrine system, contributing to the onset and progression of endocrine disorders. This review provides an overview of the crosstalk between SIRT1 and autophagy and their implications in obesity, type-2 diabetes mellitus, diabetic cardiomyopathy, and hepatic steatosis.

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Section: Sirt1-mediated Autophagy and Endocrine Disordersmentioning

confidence: 99%

SIRT1 and Autophagy: Implications in Endocrine Disorders

et al. 2022

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“…9,10 Studies have shown both the lipid metabolism and macrophage related inflammation play an essential role in regulating NASH progression. 11,12 In addition, multiple pathogenic mechanisms, including the glucose and lipid metabolism, bile acid toxicity and hepatic stellate cell activation have been reported to promote progressive liver injury during the progression of NASH. 5 Moreover, the mechanisms of hepatic lipid homeostasis are complex involving lipogenic and lipolytic genes and signaling pathways.…”

Section: Figures Introductionmentioning

confidence: 99%

Role of XBP1 in regulating the progression of non-alcoholic steatohepatitis

Wang

Zhou

et al. 2022

Journal of Hepatology

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“…Among these genes, Beclin 1 is usually known as a crucial autophagy marker for the formation of phagophores. Usually, LC3 is linked to lipids or phosphatidylethanolamine to form LC3II, which integrates into the phagophore membrane and plays an important role during autophagy ( Ajazi et al, 2021 ; da Silva Lima et al, 2021 ). Western blot analysis showed that Uro-A enhanced the expression of ULK1, LC3 and Beclin 1 compared with the control group ( Figures 3B,C ).…”

Section: Resultsmentioning

confidence: 99%

Gut Metabolite Urolithin A Inhibits Osteoclastogenesis and Senile Osteoporosis by Enhancing the Autophagy Capacity of Bone Marrow Macrophages

Tao

Yang

et al. 2022

Front. Pharmacol.

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Senile osteoporosis (SOP) is a systemic bone disease that is significantly associated with age and eventually leads to deteriorated bone strength and increased fracture risk. Urolithin A (Uro-A) is a gut microbiome-derived compound that is mainly produced from pomegranates and some nuts. Uro-A has attracted great attention in recent years in view of its protective effects on aging-related diseases, including muscle dysfunction, kidney disease and knee injury. However, its protective influence and possible mechanisms in senile osteoporosis remain unclear. Our study describes the beneficial effect of Uro-A on bone marrow macrophages (BMMs). The in vitro results demonstrated that Uro-A inhibited receptor activator for nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis in BMMs in a concentration-dependent manner. Uro-A significantly reduced the expression of osteoclast-related genes and bone resorption. Mechanistically, we found that the autophagy ability of BMMs was significantly enhanced in the early stage of Uro-A treatment, accompanied by the activation of LC3 and Beclin 1. At the same time, this enhanced autophagy activity was maintained until the later stage after stimulation with RANKL. Furthermore, we found that the MARK signaling pathway was blocked by Uro-A treatment. In a mouse model of aging, Uro-A effectively inhibited bone loss in the proximal femur, spine and tibia of aging mice. These results indicated that Uro-A is a robust and effective treatment for preventing senile osteoporosis bone loss.

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Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function

Cited by 23 publications

References 40 publications

SIRT1 and Autophagy: Implications in Endocrine Disorders

SIRT1 and Autophagy: Implications in Endocrine Disorders

Role of XBP1 in regulating the progression of non-alcoholic steatohepatitis

Gut Metabolite Urolithin A Inhibits Osteoclastogenesis and Senile Osteoporosis by Enhancing the Autophagy Capacity of Bone Marrow Macrophages

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