Non-alcoholic fatty liver disease: Immunological mechanisms and current treatments DOI Creative Commons
Lucy Petagine, Mohammed Gulrez Zariwala, Vinood B. Patel

et al.

World Journal of Gastroenterology, Journal Year: 2023, Volume and Issue: 29(32), P. 4831 - 4850

Published: Aug. 24, 2023

Non-alcoholic fatty liver disease (NAFLD) causes significant global burden and is a leading cause of mortality. NAFLD induces myriad aberrant changes in hepatocytes at both the cellular molecular level. Although spectrum widely recognised, precise triggers for progression are still to be fully elucidated. Furthermore, propagation cirrhosis poorly understood. Whilst some progress terms treatment options have been explored, an incomplete understanding hepatic alterations limits their clinical utility. We therefore reviewed key pathways responsible pathogenesis such as innate adaptative immunity, lipotoxicity fibrogenesis, highlighted current trials patients.

Language: Английский

LDL-C and TC Mediate the Risk of PNPLA3 Inhibition in Cardiovascular Diseases DOI Creative Commons
Genshan Zhang, Wei Jiang,

Fangxun He

et al.

The Journal of Clinical Endocrinology & Metabolism, Journal Year: 2024, Volume and Issue: unknown

Published: April 18, 2024

Abstract Context PNPLA3 is a promising target for the treatment of metabolic dysfunction–associated steatotic liver disease. ARO-PNPLA3 drug that efficiently lowers expression in hepatocytes at mRNA level, resulting significant reduction fat Phase I clinical trials. However, long-term effects and potential side are not well understood. Objective We conducted 2-sample, 2-step Mendelian randomization analysis to investigate association between inhibition 10 cardiovascular diseases (CVDs), as role lipid traits mediators. Methods identified genetic variants near gene, which linked percentage, instrumental variables inhibiting PNPLA3. Additionally, positive control analyses on were validate selection instruments. Results Genetically predicted significantly increased risk coronary atherosclerosis (1.14, 95% CI 1.06, 1.23), heart disease 1.08, 1.21), myocardial infarction (1.16, 1.26). Suggestive associations observed failure (1.09, 1.02, 1.17, P = .0143) atrial fibrillation (1.17, 1.00, 1.36, .0468). Blood low-density lipoprotein cholesterol (LDL-C) total (TC) mediated approximately 16% 25%, 30%, 14% 22% atherosclerosis, infarction, disease, respectively. Conclusion This study suggests increases major CVDs. Moreover, blood LDL-C TC may mediate proportion or infarction.

Language: Английский

Citations

10
Diagnostic performance of sixteen biomarkers for MASLD: A study in a Mexican cohort DOI
Bryan Adrián Priego-Parra,

Sara Alejandra Reyes-Diaz,

Héctor R. Ordaz-Álvarez

et al.

Clinics and Research in Hepatology and Gastroenterology, Journal Year: 2024, Volume and Issue: 48(7), P. 102400 - 102400

Published: June 18, 2024

Language: Английский

Citations

10
Multivitamin supplementation and its impact in metabolic dysfunction-associated steatotic liver disease DOI Creative Commons
Tom Ryu, Seung Yun Chae, Jae Jun Lee

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: March 13, 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) is an emerging global health concern with limited therapeutic options. Multivitamins, widely consumed dietary supplements, have been proposed to modulate oxidative stress and inflammation, potentially impacting MASLD progression. However, their efficacy in reducing mortality other complications remains unclear. Using data from the UK Biobank 7 years of median follow-up period, this study assessed association between multivitamin use outcomes, including all-cause mortality, liver-related cardio-cerebrovascular (CVD), chronic kidney (CKD), individuals those without disease. Inverse probability treatment weighting (IPTW) was employed adjust for confounders. Multivitamin users showed a significantly lower risk cohort both before (HR: 0.88, 95% CI 0.81–0.95, P = 0.034) after 0.94, 0.88–1.00, 0.037) IPTW adjustment. also associated CVD 0.72, 0.68–0.76, < 0.001) CKD 0.73, 0.67–0.81, cohort. No significant reduction found or cirrhosis incidence. These findings suggest that multivitamins might provide broader protective effects populations metabolic dysfunction. Further research needed clarify role liver-specific outcomes.

Language: Английский

Citations

2
Bioengineered extracellular vesicles: The path to precision medicine in liver diseases DOI Creative Commons
Ashmit Mittal,

Vibhuti R Jakhmola,

Sukriti Baweja

et al.

Liver Research, Journal Year: 2025, Volume and Issue: 9(1), P. 17 - 28

Published: Feb. 20, 2025

Language: Английский

Citations

1
Non-alcoholic fatty liver disease: Immunological mechanisms and current treatments DOI Creative Commons
Lucy Petagine, Mohammed Gulrez Zariwala, Vinood B. Patel

et al.

World Journal of Gastroenterology, Journal Year: 2023, Volume and Issue: 29(32), P. 4831 - 4850

Published: Aug. 24, 2023

Non-alcoholic fatty liver disease (NAFLD) causes significant global burden and is a leading cause of mortality. NAFLD induces myriad aberrant changes in hepatocytes at both the cellular molecular level. Although spectrum widely recognised, precise triggers for progression are still to be fully elucidated. Furthermore, propagation cirrhosis poorly understood. Whilst some progress terms treatment options have been explored, an incomplete understanding hepatic alterations limits their clinical utility. We therefore reviewed key pathways responsible pathogenesis such as innate adaptative immunity, lipotoxicity fibrogenesis, highlighted current trials patients.

Language: Английский

Citations

22