The roles of autophagy and thyroid hormone in the pathogenesis and treatment of NAFLD

Zhou, Jin; Sinha, Rohit Anthony; Yen, Paul M.

doi:10.20517/2394-5079.2021.82

Cited by 9 publications

(18 citation statements)

References 113 publications

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“…Many preclinical and clinical studies show that promoting autophagy improves hepatic steatosis, which has been reviewed recently. 45,48 Restoring the lysosome pH could be another approach to increase lysosomal degradation ability and autophagy flux. 49 Similar to increasing LAL activity, the possibility of lysosome-related lipotoxicity caused by excess lysosome degradation products needs to be evaluated.…”

Section: Autophagymentioning

confidence: 99%

“…It logically follows that with impaired autophagy in NAFLD, induction of autophagy became a potential approach for NAFLD treatment. Many preclinical and clinical studies show that promoting autophagy improves hepatic steatosis, which has been reviewed recently 45,48 . Restoring the lysosome pH could be another approach to increase lysosomal degradation ability and autophagy flux 49 .…”

Section: Autophagymentioning

confidence: 99%

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Targeting the lysosome: Mechanisms and treatments for nonalcoholic fatty liver disease

2022

J of Cellular Biochemistry

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The multiple functions of the lysosome, including degradation, nutrient sensing, signaling, and gene regulation, enable the lysosome to regulate lipid metabolism at different levels. In this review, I summarize the recent studies on lysosomal regulation of lipid metabolism and the alterations of the lysosome functions in the livers affected by nonalcoholic fatty liver disease (NAFLD). NAFLD is a highly prevalent lipid metabolic disorder. The progression of NAFLD leads to nonalcoholic steatohepatitis (NASH) and other severe liver diseases, and thus the prevention and treatments of NAFLD progression are critically needed. Targeting the lysosome is a promising strategy. I also discuss the current manipulations of the lysosome functions in the preclinical studies of NAFLD and propose my perspectives on potential future directions.

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Section: Autophagymentioning

confidence: 99%

Section: Autophagymentioning

confidence: 99%

Targeting the lysosome: Mechanisms and treatments for nonalcoholic fatty liver disease

2022

J of Cellular Biochemistry

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“…Since thyroid hormone-induced autophagy was first reported by Sinha et al in 2012 [41], numerous studies have demonstrated the close correlation between thyroid disorders and autophagy. Major topics include thyroid hormone effects on autophagic signaling (thyroid hormonemediated autophagy) [10][11][12][13], the relationship between autophagy and the development of thyroid diseases (e.g., thyroid carcinoma or autoimmune thyroid diseases) [42], and the role of autophagy in the quality control of thyrocytes [43]. In line with the first topic, our research group, among others, have identified different cargos (targets) of thyroid hormone-mediated autophagy, including lipid droplets (lipophagy), mitochondria (mitophagy), and aggregated proteins (aggrephagy) [2,12,44,45].…”

Section: Autophagy and Thyroid Hormone Statusmentioning

confidence: 99%

“…The same group also proposed Sirt1 as a novel therapeutic target for the treatment of atherosclerosis. Given that thyroid hormones induce autophagy in several cells and tissues [10][11][12][13], we deduced that thyroid hormones can promote macrophage autophagy and prevent the progression of atherosclerosis (Fig. 3).…”

Section: Autophagy and Immune Response In Atherosclerosismentioning

confidence: 99%

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Role of thyroid hormone in an experimental model of atherosclerosis: the potential mediating role of immune response and autophagy

Ohba

Iwaki

2022

Endocr J

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Accumulating evidence has revealed that several conditions related to abnormal thyroid hormone status, such as dyslipidemia, hypertension, or hypercoagulable state, can exacerbate atherosclerotic vascular disease. Thyroid hormone effects on vascular smooth muscle cells and endothelial cells have also been studied extensively. However, only limited information is available on thyroid hormone-mediated immune response in current review articles on the pathophysiology of atherosclerosis. This report thus presents an overview of the recent advances in the understanding of the dynamic interactions taking place between thyroid hormone status and immune response in the pathogenesis of atherosclerosis. In particular, we focus on macrophages and T-lymphocytes, which have been recognized as important determinants for the initiation and development of atherosclerosis. Numerous studies have revealed the role of autophagy in immune cells produced in atherosclerosis. In addition, thyroid hormones induce autophagy in several cells and tissues, such as liver, skeletal muscles, lungs, and brown adipose tissue. Our research group, among others, have reported different targets of thyroid hormonemediated autophagy, including lipid droplets (lipophagy), mitochondria (mitophagy), and aggregated proteins (aggrephagy). Based on these findings, thyroid hormone-mediated autophagy could serve as a novel therapeutic approach for atherosclerosis. We also consider the limitations of the current murine models for studies on atherosclerosis, especially in relation to lowdensity lipoprotein-cholesterol driven atherosclerotic plaque.

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A novel combination of metformin and resveratrol alleviates hepatic steatosis by activating autophagy through the cAMP/AMPK/SIRT1 signaling pathway

Noori

Zarghi

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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The roles of autophagy and thyroid hormone in the pathogenesis and treatment of NAFLD

Cited by 9 publications

References 113 publications

Targeting the lysosome: Mechanisms and treatments for nonalcoholic fatty liver disease

Targeting the lysosome: Mechanisms and treatments for nonalcoholic fatty liver disease

Role of thyroid hormone in an experimental model of atherosclerosis: the potential mediating role of immune response and autophagy

A novel combination of metformin and resveratrol alleviates hepatic steatosis by activating autophagy through the cAMP/AMPK/SIRT1 signaling pathway

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