Digestive Diseases and Sciences, Год журнала: 2024, Номер 69(4), С. 1430 - 1443
Опубликована: Март 4, 2024
Язык: Английский
Digestive Diseases and Sciences, Год журнала: 2024, Номер 69(4), С. 1430 - 1443
Опубликована: Март 4, 2024
Язык: Английский
European Journal of Heart Failure, Год журнала: 2025, Номер unknown
Опубликована: Янв. 8, 2025
Язык: Английский
Процитировано
5Acta Pharmacologica Sinica, Год журнала: 2025, Номер unknown
Опубликована: Янв. 29, 2025
Язык: Английский
Процитировано
3Cells, 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
2Environmental 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
69Frontiers 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
56Free 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
51Journal 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
50World 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
47Journal of Ethnopharmacology, Год журнала: 2023, Номер 318, С. 116927 - 116927
Опубликована: Июль 31, 2023
Язык: Английский
Процитировано
33Alimentary 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
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