Cigarette Smoke Contributes to the Progression of MASLD: From the Molecular Mechanisms to Therapy

Cells, Journal Year: 2025, Volume and Issue: 14(3), P. 221 - 221

Published: Feb. 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

Language: Английский

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Metabolic-Associated Fatty Liver Disease: The Influence of Oxidative Stress, Inflammation, Mitochondrial Dysfunctions, and the Role of Polyphenols

Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(10), P. 1354 - 1354

Published: Oct. 10, 2024

Metabolic-Associated Fatty Liver Disease (MAFLD) is a clinical-pathological scenario that occurs due to the accumulation of triglycerides in hepatocytes which considered significant cause liver conditions and contributes an increased risk death worldwide. Even though possible causes MAFLD can involve interaction genetics, hormones, nutrition, lifestyle (diet sedentary lifestyle) most influential factor developing this condition. Polyphenols comprise many natural chemical compounds be helpful managing metabolic diseases. Therefore, aim review was investigate impact oxidative stress, inflammation, mitochondrial dysfunction, role polyphenols MAFLD. Some reverse part damage related or among them are anthocyanin, baicalin, catechin, curcumin, chlorogenic acid, didymin, epigallocatechin-3-gallate, luteolin, mangiferin, puerarin, punicalagin, resveratrol, silymarin. These have actions reducing plasma enzymes, body mass index, waist circumference, adipose visceral indices, lipids, glycated hemoglobin, insulin resistance, HOMA index. They also reduce nuclear factor-KB (NF-KB), interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), blood pressure, fat content, steatosis fibrosis. On other hand, they improve HDL-c, adiponectin levels, fibrogenesis markers. results show promising prevention treatment

Language: Английский

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Bioactive Compounds Formulated in Phytosomes Administered as Complementary Therapy for Metabolic Disorders

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(8), P. 4162 - 4162

Published: April 9, 2024

Metabolic disorders (MDs), including dyslipidemia, non-alcoholic fatty liver disease, diabetes mellitus, obesity and cardiovascular diseases are a significant threat to human health, despite the many therapies developed for their treatment. Different classes of bioactive compounds, such as polyphenols, flavonoids, alkaloids, triterpenes have shown therapeutic potential in ameliorating various disorders. Most these compounds present low bioavailability when administered orally, being rapidly metabolized digestive tract which makes metabolites less effective. Moreover, some cannot fully exert beneficial properties due solubility complex chemical structure impede passive diffusion through intestinal cell membranes. To overcome limitations, an innovative delivery system phytosomes was developed. This review aims highlight scientific evidence proving enhanced benefits formulated compared free compounds. The existing knowledge concerning phytosomes’ preparation, characterization well commercially available with alleviate MDs concisely depicted. brings arguments encourage use phytosome formulation diminish risk factors inducing MDs, or treat already installed complementary therapy allopathic medication.

Language: Английский

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Quantitative imaging using [18F]F-TZ3108 to assess metabolic-associated fatty liver disease progression and low-carbohydrate diet efficacy

Nuclear Medicine and Biology, Journal Year: 2025, Volume and Issue: 144-145, P. 108997 - 108997

Published: Jan. 22, 2025

Language: Английский

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Protein kinase-mediated inhibition of autophagy by palmitic acid in hepatocytes

European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 177528 - 177528

Published: March 1, 2025

Language: Английский

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Machine learning-based disease risk stratification and prediction of metabolic dysfunction-associated fatty liver disease using vibration-controlled transient elastography: Result from NHANES 2021–2023

BMC Gastroenterology, Journal Year: 2025, Volume and Issue: 25(1)

Published: April 14, 2025

Language: Английский

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Galectin-3 and Severity of Liver Fibrosis in Metabolic Dysfunction-Associated Fatty Liver Disease

Protein and Peptide Letters, Journal Year: 2024, Volume and Issue: 31(4), P. 290 - 304

Published: April 1, 2024

Abstract: Metabolic dysfunction-associated Fatty Liver Disease (MAFLD) is a chronic liver disease characterized by the accumulation of fat in and hepatic steatosis, which can progress to critical conditions, including Steatohepatitis (MASH), fibrosis, cirrhosis, hepatocellular carcinoma. Galectin-3, member galectin family proteins, has been involved cascades that are responsible for pathogenesis progression fibrosis MAFLD. This review summarizes present understanding role galectin-3 severity MAFLD its associated fibrosis. The article assesses underlying galectin-3-mediated fibrogenesis, triggering stellate cells, regulation extracellular degradation, modulation immune reactions responses. It also highlights assessments potential diagnostic therapeutic implications during Overall, this provides insights into multifaceted interaction between MAFLD, could lead development novel strategies diagnosis treatment prevalent disease.

Language: Английский

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Metabolic dysfunction-associated fatty liver disease/metabolic dysfunction-associated steatotic liver disease: general provisions

CHILD`S HEALTH, Journal Year: 2024, Volume and Issue: 19(2), P. 107 - 116

Published: April 24, 2024

The literature review deals with the problem of metabolic dysfunction-associated fatty liver disease that is poorly studied in pediatric gastroenterology. Until recently, primary hepatic steatosis not associated alcohol intake was defined as non-alcoholic disease. Given unity pathogenetic mechanisms underlying steatosis, steatohepatitis, fibrosis disorders, such visceral obesity, insulin resistance, meta-inflammation adipose tissue, it proposed to change terminology. authors present data on modern nomenclature definitions, etiological factors, prevalence, criteria disorders and this nosology specific childhood. Metabolic nonalcoholic are characterized by development hepatosteatosis. However, a distinguishing feature presence patient. It believed use term “metabolic disease” clinical practice allows doctors make diagnosis more reliably accurately modify patient’s lifestyle. Much attention paid description heterogeneity practice, concise list therapeutic options for childhood presented.

Language: Английский

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Mitochondria-targeted hydrogen sulfide donor reduces fatty liver and obesity in mice fed a high fat diet by inhibiting de novo lipogenesis and inflammation via mTOR/SREBP-1 and NF-κB signaling pathways

Pharmacological Research, Journal Year: 2024, Volume and Issue: 209, P. 107428 - 107428

Published: Sept. 19, 2024

Language: Английский

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NAT10 promotes liver lipogenesis in mouse through N4-acetylcytidine modification of Srebf1 and Scap mRNA

Lipids in Health and Disease, Journal Year: 2024, Volume and Issue: 23(1)

Published: Nov. 11, 2024

Metabolic dysfunction associated steatotic liver disease (MASLD), closely linked to excessive lipogenesis, induces chronic disease. MASLD often cause other metabolic diseases, such as cardiovascular disease, diabetes and obesity. However, the mechanism of N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) mRNA modification in lipogenesis has not been fully elucidated. This study investigated role NAT10 targeting ac4C modification. The expression mouse was assessed after a 12-week high-fat diet. In addition, also detected AML12 hepatocytes cells were treated with 150 µmol/L palmitic acid (PA). performed by dot blotting. Oil red O staining Srebf1, Acaca Fasn used assess overexpression or knockdown. acRIP-PCR RIP-PCR verify Srebf1 Scap NAT10. Furthermore, evaluated AAV-mediated target knockdown treating specific inhibitor, Remodelin. revealed that is significantly upregulated drastically increased PA. Silencing notably inhibited liver. NAT10-RIP-PCR modified mRNA, critical modulator regulate lipogenesis. Besides, Remodelin strongly including TG, serum ALT, AST, TG TC level glucose metabolism. mediates thereby affecting provided new for treatment MASLD.

Language: Английский

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