Autophagy and the unfolded protein response shape the non-alcoholic fatty liver landscape: decoding the labyrinth

Dashti, Zahra; Yousefi, Zeynab; Kiani, Pouria; Taghizadeh, Motahareh; Maleki, Mohammad Hasan; Borji, Mohammad; Vakili, Omid; Shafiee, Sayed Mohammad

doi:10.1016/j.metabol.2024.155811

Cited by 7 publications

(2 citation statements)

References 188 publications

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“…Currently, the treatment for NAFLD is based on dietary control, physical activity, and surgical weight loss, but the UPR has recently been proven to be an ideal target for various drugs aimed at alleviating the progression of NAFLD. This underscores the significant research value of studying ERS and its UPR branches' mechanisms (126,127).…”

Section: Discussionmentioning

confidence: 89%

Endoplasmic reticulum stress: bridging inflammation and obesity-associated adipose tissue

Ma,

Zhang,

Zhao

et al. 2024

Front. Immunol.

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Obesity presents a significant global health challenge, increasing the susceptibility to chronic conditions such as diabetes, cardiovascular disease, and hypertension. Within the context of obesity, lipid metabolism, adipose tissue formation, and inflammation are intricately linked to endoplasmic reticulum stress (ERS). ERS modulates metabolism, insulin signaling, inflammation, as well as cell proliferation and death through the unfolded protein response (UPR) pathway. Serving as a crucial nexus, ERS bridges the functionality of adipose tissue and the inflammatory response. In this review, we comprehensively elucidate the mechanisms by which ERS impacts adipose tissue function and inflammation in obesity, aiming to offer insights into targeting ERS for ameliorating metabolic dysregulation in obesity-associated chronic diseases such as hyperlipidemia, hypertension, fatty liver, and type 2 diabetes.

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Section: Discussionmentioning

confidence: 89%

Endoplasmic reticulum stress: bridging inflammation and obesity-associated adipose tissue

Ma,

Zhang,

Zhao

et al. 2024

Front. Immunol.

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“…Patients with NAFL are clinically asymptomatic, and NAFL may progress to NAFLD and liver fibrosis, with an elevated risk of cirrhosis and hepatocellular carcinoma [4]. However, the underlying molecular mechanism for the development of NAFL and the subsequent advances to later stages of liver diseases remains unclear [5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Accumulation of Non-Pathological Liver Fat Is Associated with the Loss of Glyoxalase I Activity in Humans

Peter,

Schleicher,

Kliemank

et al. 2024

Metabolites

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The underlying molecular mechanisms for the development of non-alcoholic fatty liver (NAFL) and its progression to advanced liver diseases remain elusive. Glyoxalase 1 (Glo1) loss, leading to elevated methylglyoxal (MG) and dicarbonyl stress, has been implicated in various diseases, including obesity-related conditions. This study aimed to investigate changes in the glyoxalase system in individuals with non-pathological liver fat. Liver biopsies were obtained from 30 individuals with a narrow range of BMI (24.6–29.8 kg/m2). Whole-body insulin sensitivity was assessed using HOMA-IR. Liver biopsies were analyzed for total triglyceride content, Glo1 and Glo2 mRNA, protein expression, and activity. Liquid chromatography–tandem mass spectrometry determined liver dicarbonyl content and oxidation and glycation biomarkers. Liver Glo1 activity showed an inverse correlation with HOMA-IR and liver triglyceride content, but not BMI. Despite reduced Glo1 activity, no associations were found with elevated liver dicarbonyls or glycation markers. A sex dimorphism was observed in Glo1, with females exhibiting significantly lower liver Glo1 protein expression and activity, and higher liver MG-H1 content compared to males. This study demonstrates that increasing liver fat, even within a non-pathological range, is associated with reduced Glo1 activity.

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CTRP9 alleviates diet induced obesity through increasing lipolysis mediated by enhancing autophagy-initiation complex formation.

Lei,

Li,

Zuo

et al. 2024

The Journal of Nutritional Biochemistry

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Autophagy and the unfolded protein response shape the non-alcoholic fatty liver landscape: decoding the labyrinth

Cited by 7 publications

References 188 publications

Endoplasmic reticulum stress: bridging inflammation and obesity-associated adipose tissue

Endoplasmic reticulum stress: bridging inflammation and obesity-associated adipose tissue

Accumulation of Non-Pathological Liver Fat Is Associated with the Loss of Glyoxalase I Activity in Humans

CTRP9 alleviates diet induced obesity through increasing lipolysis mediated by enhancing autophagy-initiation complex formation.

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