Insulin Resistance/Sensitivity Measures as Screening Indicators of Metabolic-Associated Fatty Liver Disease and Liver Fibrosis DOI
Mohammad E. Khamseh, Mojtaba Malek, Soodeh Jahangiri

и другие.

Digestive Diseases and Sciences, Год журнала: 2024, Номер 69(4), С. 1430 - 1443

Опубликована: Март 4, 2024

Язык: Английский

Metabolic dysfunction‐associated steatotic liver disease is associated with increased risks of heart failure DOI Open Access
Kai‐Chun Chang, Tung‐Hung Su, Cho‐Kai Wu

и другие.

European Journal of Heart Failure, Год журнала: 2025, Номер unknown

Опубликована: Янв. 8, 2025

Язык: Английский

Процитировано

5

Apolipoprotein B100 acts as a tumor suppressor in ovarian cancer via lipid/ER stress axis-induced blockade of autophagy DOI

Zeyuan Yin,

Shi-min He,

Xinyuan Zhang

и другие.

Acta Pharmacologica Sinica, Год журнала: 2025, Номер unknown

Опубликована: Янв. 29, 2025

Язык: Английский

Процитировано

3

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

2

Mitochondria-Dependent Oxidative Stress Mediates ZnO Nanoparticle (ZnO NP)-Induced Mitophagy and Lipotoxicity in Freshwater Teleost Fish DOI

Guang‐Hui Chen,

Chang-Chun Song,

Tao Zhao

и другие.

Environmental Science & Technology, Год журнала: 2022, Номер 56(4), С. 2407 - 2420

Опубликована: Фев. 2, 2022

Due to many special characteristics, zinc oxide nanoparticles (ZnO NPs) are widely used all over the world, leading their wide distribution in environment. However, toxicities and mechanisms of environmental ZnO NP-induced changes physiological processes metabolism remain largely unknown. Here, we found that addition dietary NPs disturbed hepatic Zn metabolism, increased lipid accumulation, downregulated lipolysis, induced oxidative stress, activated mitophagy; N,N,N',N'-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, Zn2+ ions chelator) alleviated high mitophagy. Mechanistically, suppression mitochondrial stress attenuated NP-activated mitophagy lipotoxicity. Taken together, our study elucidated mediated lipotoxicity; could be dissociated free ions, which partially contributed mitophagy, metabolism. Our provides novel insights into impacts mechanism as harmful substances inducing lipotoxicity aquatic organisms, accordingly, metabolism-relevant parameters will useful for risk assessment nanoparticle materials

Язык: Английский

Процитировано

69

Emerging Role of Hepatic Ketogenesis in Fatty Liver Disease DOI Creative Commons

Raja Gopal Reddy Mooli,

Sadeesh K. Ramakrishnan

Frontiers in Physiology, Год журнала: 2022, Номер 13

Опубликована: Июль 4, 2022

Non-alcoholic fatty liver disease (NAFLD), the most common chronic diseases, arise from non-alcoholic (NAFL) characterized by excessive fat accumulation as triglycerides. Although NAFL is benign, it could progress to steatohepatitis (NASH) manifested with inflammation, hepatocyte damage and fibrosis. A subset of NASH patients develops end-stage diseases such cirrhosis hepatocellular carcinoma. The pathogenesis NAFLD highly complex strongly associated perturbations in lipid glucose metabolism. Lipid disposal pathways, particular, impairment condensation acetyl-CoA derived β-oxidation into ketogenic pathway influence hepatic loads Current evidence suggests that ketogenesis dispose up two-thirds lipids entering liver, its dysregulation significantly contribute pathogenesis. Moreover, ketone body administration mice humans shows a significant improvement NAFLD. This review focuses on role We possible mechanisms through which impaired may promote progression. Finally, sheds light therapeutic implications diet

Язык: Английский

Процитировано

56

Nonalcoholic steatohepatitis and mechanisms by which it is ameliorated by activation of the CNC-bZIP transcription factor Nrf2 DOI Creative Commons

Boushra Bathish,

Holly Robertson, John Dillon

и другие.

Free Radical Biology and Medicine, Год журнала: 2022, Номер 188, С. 221 - 261

Опубликована: Июнь 18, 2022

Non-alcoholic steatohepatitis (NASH) represents a global health concern. It is characterised by fatty liver, hepatocyte cell death and inflammation, which are associated with lipotoxicity, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, iron overload oxidative stress. NF-E2 p45-related factor 2 (Nrf2) transcription that combats Remarkably, Nrf2 downregulated during the development of NASH, probably accelerates disease, whereas in pre-clinical studies upregulation inhibits NASH. We now review scientific literature proposes downregulation NASH involves its increased ubiquitylation proteasomal degradation, mediated Kelch-like ECH-associated protein 1 (Keap1) and/or β-transducin repeat-containing (β-TrCP) HMG-CoA reductase degradation (Hrd1, also called synoviolin (SYVN1)). Additionally, Nrf2-mediated may involve diminished recruitment coactivators Nrf2, due to levels activating 3 (ATF3) nuclear factor-kappaB (NF-κB) p65, or competition for promoter binding BTB CNC homology (Bach1). Many processes downregulate triggered transforming growth factor-beta (TGF-β), stress amplifying signalling. Oxidative increase suppression β-TrCP through facilitating formation DSGIS-containing phosphodegron glycogen synthase kinase-3. In animal models, knockout increases susceptibility while pharmacological activation inducing agents target Keap1 These counter affected β-TrCP, Hrd1/SYVN1, ATF3, NF-κB p65 Bach1, suppressing Activation likely inhibit ameliorating ER overload. Crucially, mice has already been established supresses liver steatosis inflammation. There therefore compelling evidence provides comprehensive multipronged strategy treat

Язык: Английский

Процитировано

51

The Role of Insulin Resistance in Fueling NAFLD Pathogenesis: From Molecular Mechanisms to Clinical Implications DOI Open Access
Rossella Palma, Annamaria Pronio, Mario Romeo

и другие.

Journal of Clinical Medicine, Год журнала: 2022, Номер 11(13), С. 3649 - 3649

Опубликована: Июнь 24, 2022

Non-alcoholic fatty liver disease (NAFLD) represents a predominant hepatopathy that is rapidly becoming the most common cause of hepatocellular carcinoma worldwide. The close association with metabolic syndrome’s extrahepatic components has suggested nature systemic metabolic-related disorder based on interplay between genetic, nutritional, and environmental factors, creating complex network yet-unclarified pathogenetic mechanisms in which role insulin resistance (IR) could be crucial. This review detailed clinical evidence involved NAFLD–IR relationship, presenting both classic more innovative models. In particular, we focused reciprocal effects IR, oxidative stress, inflammation insulin-sensitivity disruption critical regions such as hepatic adipose tissue, while considering impact genetics/epigenetics regulation IR well nutrients specific insulin-related gene expression (nutrigenetics nutrigenomics). addition, discussed emerging capability gut microbiota to interfere physiological signaling hormonal pathways responsible for maintaining homeostasis by inducing an abnormal activation immune system. translation these novel findings into practice promote expansion accurate diagnostic/prognostic stratification tools tailored pharmacological approaches.

Язык: Английский

Процитировано

50

Nuclear factor erythroid 2-related factor 2-mediated signaling and metabolic associated fatty liver disease DOI Creative Commons
Vidyasagar Naik Bukke, Archana Moola, Gaetano Serviddio

и другие.

World Journal of Gastroenterology, Год журнала: 2022, Номер 28(48), С. 6909 - 6921

Опубликована: Дек. 26, 2022

Oxidative stress is a key driver in the development and progression of several diseases, including metabolic associated fatty liver disease (MAFLD). This condition includes wide spectrum pathological injuries, extending from simple steatosis to inflammation, fibrosis, cirrhosis, hepatocellular carcinoma. Excessive buildup lipids strictly related oxidative MAFLD, progressing fibrosis cirrhosis. The nuclear factor erythroid 2-related 2 (NRF2) master regulator redox homeostasis. NRF2 plays an important role for cellular protection by inducing expression genes antioxidant, anti-inflammatory, cytoprotective response. Consistent evidence demonstrates that involved every step MAFLD deve-lopment, advanced ini-tiation/progression activators regulate lipid metabolism alleviating genes. Thus, modulating activation crucial not only understanding specific mechanisms underlying but also characterize effective therapeutic strategies. review outlined current knowledge on effects pathway, modulators, implications steatosis, MAFLD.

Язык: Английский

Процитировано

47

Chinese herbal medicines: The modulator of nonalcoholic fatty liver disease targeting oxidative stress DOI
Pin Gong, Hui Long, Yuxi Guo

и другие.

Journal of Ethnopharmacology, Год журнала: 2023, Номер 318, С. 116927 - 116927

Опубликована: Июль 31, 2023

Язык: Английский

Процитировано

33

Global perspective on nonalcoholic fatty liver disease and nonalcoholic steatohepatitis ‐ prevalence, clinical impact, economic implications and management strategies DOI Open Access
Pegah Golabi, Soroor Owrangi, Zobair M. Younossi

и другие.

Alimentary Pharmacology & Therapeutics, Год журнала: 2024, Номер 59(S1)

Опубликована: Май 30, 2024

Summary Background The metabolically‐based liver disease, nonalcoholic fatty disease (NAFLD), is the most common cause of chronic currently affecting 38% world's adult population. NAFLD can be progressive leading to steatohepatitis (NASH), transplantation, cancer, liver‐related mortality and associated with decreased quality life from impaired physical functioning increased healthcare resource utilisation. However, screening for cost‐prohibitive but high risk (NAFLD F2 fibrosis or greater) imperative. Aim To review global perspective on NASH Methods We retrieved articles PubMed using search terms NAFLD, prevalence, clinical burden, economic burden management strategies. Results NAFLD/NASH shows geographical variation across globe. Highest prevalence rates are in South America Middle East North Africa; lowest Africa. NAFLD's impact direct indirect medical costs loss worker productivity. It projected that, over next two decades, total cost diabetes will exceed $1.5 trillion (USD). Risk stratification algorithms identifying “high NAFLD” were made following non‐invasive tests identification development. These should used primary care endocrinology settings so timely appropriate interventions (lifestyle cardiometabolic factor management) initiated. Conclusions reduce burgeoning NAFLD/NASH, include accurate patients, linkage settings, initiation effective treatment regimens.

Язык: Английский

Процитировано

18