New Insights into AMPK, as a Potential Therapeutic Target in Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatic Fibrosis DOI Creative Commons

Hoon An,

Yerin Jang,

Jung-In Choi

и другие.

Biomolecules & Therapeutics, Год журнала: 2024, Номер unknown

Опубликована: Дек. 20, 2024

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into fibrosis and fundamentally improve function. The broad spectrum pathways regulated by AMPK makes them promising alternatives conventional replacement therapies limited pharmacological treatments currently available. In this study, we aim illustrate newly detailed multiple mechanisms MASLD based on multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance imbalance, initiates inflammatory cascades, gut dysbiosis, accumulation toxic metabolites, ultimately promoting accelerating irreversible hepatocellular carcinoma (HCC). plays a multifaceted protective role against these pathological conditions regulating several key downstream signaling pathways. It regulates biological effectors critical responses, such as SIRT1, Nrf2, mTOR, TGF-β, through complex interrelated mechanisms. Due intricate connections, AMPK's is pivotal in managing disorders. review, demonstrate specific roles its related Several agents directly activate binding agonists, while some others indirectly modulating upstream molecules, including adiponectin, LKB1, AMP: ATP ratio. As can target each stage progression, development offers immense expand therapeutic strategies diseases MASH, MASLD, fibrosis.

Язык: Английский

Cigarette Smoke Contributes to the Progression of MASLD: From the Molecular Mechanisms to Therapy DOI Creative Commons
Jihao Xu, Yifan Li,

Zhaolan Feng

и другие.

Cells, Год журнала: 2025, Номер 14(3), С. 221 - 221

Опубликована: Фев. 4, 2025

Cigarette smoke (CS), an intricate blend comprising over 4000 compounds, induces abnormal cellular reactions that harm multiple tissues. Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic (CLD), encompassing non-alcoholic (NAFL), steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). Recently, the term NAFLD has been changed to metabolic dysfunction-associated steatotic (MASLD), NASH renamed (MASH). A multitude of experiments have confirmed association between CS incidence progression MASLD. However, specific signaling pathways involved need be updated with new scientific discoveries. exposure can disrupt lipid metabolism, induce inflammation apoptosis, stimulate fibrosis through promote Currently, there no officially approved efficacious pharmaceutical intervention in clinical practice. Therefore, lifestyle modifications emerged as primary therapeutic approach for managing Smoking cessation application series natural ingredients shown ameliorate pathological changes induced by CS, potentially serving effective decelerating MASLD development. This article aims elucidate which smoking promotes MASLD, while summarizing reversal factors identified recent studies, thereby offering novel insights future research on treatment

Язык: Английский

Процитировано

1
Sea buckthorn triterpenic acids alleviates metabolic dysfunction-associated steatotic liver disease via modulation of liver biochemistry, lipid metabolism and AMPK/Nrf2/NF-κB signaling pathway DOI

Lichengcheng Ren,

Yongjing Xie,

Ruinan Wang

и другие.

Food Bioscience, Год журнала: 2025, Номер unknown, С. 106611 - 106611

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
New Insights into AMPK, as a Potential Therapeutic Target in Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatic Fibrosis DOI Creative Commons

Hoon An,

Yerin Jang,

Jung-In Choi

и другие.

Biomolecules & Therapeutics, Год журнала: 2024, Номер unknown

Опубликована: Дек. 20, 2024

AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into fibrosis and fundamentally improve function. The broad spectrum pathways regulated by AMPK makes them promising alternatives conventional replacement therapies limited pharmacological treatments currently available. In this study, we aim illustrate newly detailed multiple mechanisms MASLD based on multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance imbalance, initiates inflammatory cascades, gut dysbiosis, accumulation toxic metabolites, ultimately promoting accelerating irreversible hepatocellular carcinoma (HCC). plays a multifaceted protective role against these pathological conditions regulating several key downstream signaling pathways. It regulates biological effectors critical responses, such as SIRT1, Nrf2, mTOR, TGF-β, through complex interrelated mechanisms. Due intricate connections, AMPK's is pivotal in managing disorders. review, demonstrate specific roles its related Several agents directly activate binding agonists, while some others indirectly modulating upstream molecules, including adiponectin, LKB1, AMP: ATP ratio. As can target each stage progression, development offers immense expand therapeutic strategies diseases MASH, MASLD, fibrosis.

Язык: Английский

Процитировано

3