The Journal of Nutritional Biochemistry, Journal Year: 2024, Volume and Issue: 128, P. 109626 - 109626
Published: March 26, 2024
Language: Английский
The Journal of Nutritional Biochemistry, Journal Year: 2024, Volume and Issue: 128, P. 109626 - 109626
Published: March 26, 2024
Language: Английский
Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)
Published: Feb. 28, 2025
Language: Английский
Citations
3Antioxidants, Journal Year: 2024, Volume and Issue: 13(8), P. 906 - 906
Published: July 26, 2024
Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty (NAFLD), encompasses a range of conditions from steatosis to steatohepatitis (NASH). Its prevalence, especially among patients with metabolic syndrome, highlights its growing global impact. The pathogenesis MASLD involves dysregulation, inflammation, oxidative stress, genetic factors and, notably, mitochondrial dysfunction. Recent studies underscore the critical role dysfunction in MASLD's progression. Therapeutically, enhancing function has gained interest, along lifestyle changes and pharmacological interventions targeting processes. FDA's approval resmetirom for metabolic-associated (MASH) fibrosis marks significant step. While represents progress, further research is essential understand MASLD-related fully. Innovative strategies like gene editing small-molecule modulators, alongside interventions, can potentially improve treatment. Drug repurposing new targets will advance therapy, addressing increasing burden. Therefore, this review aims provide better understanding identify more effective preventive treatment strategies.
Language: Английский
Citations
14Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2024, Volume and Issue: unknown
Published: June 11, 2024
Language: Английский
Citations
7Journal of Chromatography B, Journal Year: 2025, Volume and Issue: unknown, P. 124563 - 124563
Published: March 1, 2025
Language: Английский
Citations
0Nutrition Reviews, Journal Year: 2025, Volume and Issue: unknown
Published: April 15, 2025
Abstract Adipose tissue serves as a dynamic endocrine organ that is pivotal in metabolic regulation. Augmenting mitochondrial activity within this holds promise combating obesity. Mitochondrial function intricately modulated by diverse fatty acid compositions. This comprehensive review aimed to elucidate the molecular mechanisms underlying dysfunction induced various profiles. While saturated acids (SFAs) pose threat integrity, polyunsaturated (PUFAs), notably n-3, mitigate SFA-induced damage, concurrently regulating thermogenic gene expression. With regard monounsaturated (MUFAs), their impact on adipose remains relatively unexplored. Although human studies are imperative for insights, prioritizing consumption of n-3 and MUFAs has emerged strategic approach, potentially enhancing biogenesis pathways. synthesis underscores critical need further investigation differential effects types mitochondria, offering potential avenues obesity intervention.
Language: Английский
Citations
0Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: April 17, 2024
Hepatic Ischemia-Reperfusion Injury (HIRI) is a major complication in liver transplants and surgeries, significantly affecting postoperative outcomes. The role of mitophagy, essential for removing dysfunctional mitochondria maintaining cellular balance, remains unclear HIRI.
Language: Английский
Citations
3Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: 400, P. 111166 - 111166
Published: July 27, 2024
Smoking is a well-established risk factor for several oral diseases, including cancer, leukoplakia and periodontitis, primarily related to reactive oxygen species (ROS). SS-31, mitochondria-targeting tetrapeptide, has exhibited demonstrable efficacy in medical conditions by attenuating mitochondrial ROS production. However, its potential the treatment of diseases remains underexplored. The aim this study was investigate therapeutic SS-31 mitigating smoking-induced epithelial injury. Through vitro experiments, our results indicate that plays protective role against cigarette smoke extract (CSE) reducing oxidative stress, inflammatory response, restoring function. Furthermore, we found mitophagy, regulated PINK1 (PTEN-induced putative kinase 1)/Parkin (Parkin RBR E3 ubiquitin-protein ligase), critical SS-31. Our findings offer valuable insights into SS-31's CSE-induced dysfunction cells. This provides novel intervention targets smoking-related diseases.
Language: Английский
Citations
3World Journal of Gastroenterology, Journal Year: 2025, Volume and Issue: 31(10)
Published: Feb. 26, 2025
BACKGROUND Insulin resistance, lipotoxicity, and mitochondrial dysfunction contribute to the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). Mitochondrial impairs oxidative phosphorylation increases reactive oxygen species production, leading steatohepatitis hepatic fibrosis. Artificial intelligence (AI) is a potent tool for diagnosis risk stratification. AIM To investigate DNA polymorphisms in susceptibility MASLD establish an AI model screening. METHODS Multiplex polymerase chain reaction was performed comprehensively genotype 82 variants screening dataset (n = 264). The significant single nucleotide polymorphism validated independent cohort 1046) using Taqman® allelic discrimination assay. Random forest, eXtreme gradient boosting, Naive Bayes, logistic regression algorithms were employed construct MASLD. RESULTS In dataset, only mt12361A>G significantly associated with showed borderline significance patients 2-3 cardiometabolic traits compared controls validation (P 0.055). Multivariate analysis confirmed that factor [odds ratio (OR) 2.54, 95% confidence interval (CI): 1.19-5.43, P 0.016]. genetic effect non-diabetic group but not diabetic group. mt12361G carriers had 2.8-fold higher than A (OR 2.80, 95%CI: 1.22-6.41, 0.015). By integrating clinical features mt12361A>G, random forest outperformed other detecting [training area under receiver operating characteristic curve (AUROC) 1.000, AUROC 0.876]. CONCLUSION variant increased severity patients. supports management primary care settings.
Language: Английский
Citations
0European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 177693 - 177693
Published: May 1, 2025
Language: Английский
Citations
0Biomolecules, Journal Year: 2025, Volume and Issue: 15(5), P. 670 - 670
Published: May 6, 2025
Cardiomyopathies comprise a heterogeneous group of cardiac disorders characterized by structural and functional abnormalities in the absence significant coronary artery disease, hypertension, valvular or congenital defects. Major subtypes include hypertrophic, dilated, arrhythmogenic, stress-induced cardiomyopathies. Oxidative stress (OS), resulting from an imbalance between reactive oxygen species (ROS) production antioxidant defenses, has emerged as key contributor to pathogenesis these conditions. ROS-mediated injury drives inflammation, protease activation, mitochondrial dysfunction, cardiomyocyte damage, thereby promoting remodeling decline. Although numerous studies implicate OS cardiomyopathy progression, precise molecular mechanisms remain incompletely defined. This review provides updated synthesis current findings on OS-related signaling pathways across subtypes, emphasizing emerging therapeutic targets within redox-regulatory networks. A deeper understanding may guide development targeted strategies improve clinical outcomes affected patients.
Language: Английский
Citations
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