Histopathology of MASLD: Insights into Liver Tissue Changes DOI
Sven Francque, Ann Driessen

Опубликована: Янв. 1, 2024

Язык: Английский

Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: A nationwide cohort study DOI Creative Commons
Seogsong Jeong, Yun Hwan Oh, Joseph Ahn

и другие.

Clinical and Molecular Hepatology, Год журнала: 2024, Номер 30(3), С. 487 - 499

Опубликована: Май 7, 2024

Background/Aims: To determine the association between evolutionary changes in metabolic dysfunction-associated steatotic liver disease (MASLD) status and risk of hepatocellular carcinoma (HCC) a nationwide population-based cohort.Methods: Information on study participants was derived from Korea National Health Insurance Service database. The population consisted 5,080,410 who underwent two consecutive biennial health screenings 2009 2012. All were followed up until HCC, death, or 31 December 2020. MASLD status, as assessed by fatty index cardiometabolic factors, including persistent non-MASLD, resolved MASLD, incident with HCC evaluated using multivariable-adjusted Cox proportional hazards regression.Results: Among 39,910,331 person-years follow-up, 4,801 developed HCC. incidence resolved, incident, approximately 2.2-, 2.3-, 4.7-fold higher, respectively, than that those non-MASLD among Korean adult population. When stratifying according to change (adjusted hazard ratio [aHR], 2.94; 95% confidence interval [CI], 2.68–3.21; P<0.001), (aHR, 1.85; CI, 1.63–2.10; 1.33; 1.18–1.50; P<0.001) had an increased compared non-MASLD.Conclusions: associated differential independent factors concomitant medications, providing additional information stratification patients MASLD.

Язык: Английский

Процитировано

9

Galangin alleviated Doxorubicin-induced cardiotoxicity by inhibiting ferroptosis through GSTP1/JNK pathway DOI

Guangjie Shu,

Ke Chen, Junyan Li

и другие.

Phytomedicine, Год журнала: 2024, Номер 134, С. 155989 - 155989

Опубликована: Авг. 31, 2024

Язык: Английский

Процитировано

5

MEF2C Alleviates Postoperative Cognitive Dysfunction by Repressing Ferroptosis DOI Creative Commons
Shanshan Wang,

Zankai Wu,

Xueshan Bu

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(10)

Опубликована: Сен. 30, 2024

Ferroptosis, a form of programmed cell death featured by lipid peroxidation, has been proposed as potential etiology for postoperative cognitive dysfunction (POCD). Myocyte-specific enhancer factor 2C (MEF2C), transcription expressed in various brain types, implicated disorders. This study sought to ascertain whether MEF2C governs capacity affecting ferroptosis.

Язык: Английский

Процитировано

5

Exploring the Role of Metabolic Hyperferritinaemia (MHF) in Steatotic Liver Disease (SLD) and Hepatocellular Carcinoma (HCC) DOI Open Access
Nikolaos-Andreas Anastasopoulos, Alexandra Barbouti, Anna Goussia

и другие.

Cancers, Год журнала: 2025, Номер 17(5), С. 842 - 842

Опубликована: Фев. 28, 2025

The increasing prevalence of the spectrum Steatotic Liver Disease (SLD), including Metabolic-Associated (MASLD), Steatohepatitis (MASH), and progression to Cirrhosis Hepatocellular Carcinoma (HCC) has led intense research in disease pathophysiology, with many studies focusing on role iron. Iron overload, which is often observed patients SLD as a part metabolic hyperferritinaemia (MHF), particularly reticuloendothelial system (RES), can exacerbate steatosis. This imbalance iron distribution, coupled high-fat diet, further promote by means oxidative stress triggering inflammation activating hepatic stellate cells (HSCs), therefore leading fibrosis simple steatosis more severe MASH. influence overload also been shown complex ferroptosis, type cell death driven iron-dependent lipid peroxidation. Ferroptosis depletes liver's antioxidant capacity, contributing development MASH, while its MASH-related HCC potentially linked alternations tumour microenvironment, well ferroptosis resistance. iron-rich steatotic environment becomes prone hepatocarcinogenesis activation several pro-carcinogenic mechanisms epithelial-to-mesenchymal transition deactivation DNA damage repair. Biochemical markers deranged metabolism have all stages associated multiple patient cohorts diverse genetic backgrounds, enhancing our daily clinical understanding this interaction. Further could lead enhanced therapies for management prevention.

Язык: Английский

Процитировано

0

From mechanisms to medicine: Ferroptosis as a Therapeutic target in liver disorders DOI Creative Commons
Yuqi He,

Yumeng Lin,

Jinfeng Song

и другие.

Cell Communication and Signaling, Год журнала: 2025, Номер 23(1)

Опубликована: Март 7, 2025

In recent 10 years, ferroptosis has become a hot research direction in the scientific community as new way of cell death. Iron toxicity accumulation and lipotoxicity are unique features. Several studies have found that is involved regulation hepatic microenvironment various metabolisms, thereby mediating progression related liver diseases. For example, NRF2 FSP1, important regulatory proteins ferroptosis, development tumors failure. this manuscript, we present mechanisms concern with addition, summarize clinical advances targeted therapy for We expect manuscript can provide perspective treatment

Язык: Английский

Процитировано

0

A Comprehensive Review of Metabolic Dysfunction-Associated Steatotic Liver Disease: Its Mechanistic Development Focusing on Methylglyoxal and Counterbalancing Treatment Strategies DOI Open Access
Izabela Berdowska, M. Matusiewicz, Izabela Fecka

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2394 - 2394

Опубликована: Март 7, 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a multifactorial disorder characterized by excessive lipid accumulation in the which dysregulates organ’s function. The key contributor to MASLD development insulin resistance (IR) affects many organs (including adipose tissue, skeletal muscles, and liver), whereas molecular background associated with oxidative, nitrosative, carbonyl stress. Among molecules responsible for stress effects, methylglyoxal (MGO) seems play major pathological MGO—a by-product of glycolysis, fructolysis, lipolysis (from glycerol fatty acids-derived ketone bodies)—is implicated hyperglycemia, hyperlipidemia, obesity, type 2 diabetes, hypertension, cardiovascular diseases. Its causative effect stimulation prooxidative proinflammatory pathways has been well documented. Since metabolic dysregulation leading these pathologies promotes MASLD, role MGO addressed this review. Potential participation mechanism discussed regard its different signaling routes events accelerating disorder. Moreover, treatment strategies including approved potential therapies are overviewed them, medications aimed at attenuating MGO-induced processes addressed.

Язык: Английский

Процитировано

0

Lipid metabolism analysis reveals that DGAT1 regulates Th17 survival by controlling lipid peroxidation in uveitis DOI Creative Commons
Tianfu Wang, Runping Duan, Zhaohuai Li

и другие.

JCI Insight, Год журнала: 2025, Номер 10(7)

Опубликована: Апрель 7, 2025

Lipid metabolism is closely linked with antitumor immunity and autoimmune disorders. However, the precise role of lipid in uveitis pathogenesis not clear. In our study, we analyzed single-cell RNA-Seq (scRNA-Seq) data from cervical draining lymph nodes (CDLNs) mice experimental (EAU), revealing an increased abundance fatty acids Th17 cells. Subsequent scRNA-Seq analysis identified upregulation DGAT1 expression EAU its marked reduction under various immunosuppressive agents. Suppression prevented conversion into neutral droplets, resulting accumulation peroxidation subsequent proportion Inhibiting by Ferrostatin-1 effectively restored cell numbers that were decreased inhibitor. Moreover, validated CD4+ T cells patients Vogt-Koyanagi-Harada (VKH) disease, a human uveitis. induced reduced Collectively, study focused on elucidating regulatory mechanisms underlying survival proposed targeting may hold promise as therapeutic approach for

Язык: Английский

Процитировано

0

Antifibrotic Therapies for Metabolic Dysfunction-associated Steatotic Liver Disease DOI Creative Commons
Robert F. Schwabe, Frank Tacke, Atsushi Sugimoto

и другие.

JHEP Reports, Год журнала: 2025, Номер unknown, С. 101421 - 101421

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0

Combined exposure of polystyrene nanoplastics and silver nanoparticles exacerbating hepatotoxicity in zebrafish mediated by ferroptosis pathway through increased silver accumulation DOI
Ying Cheng, Ziyi Fan,

Ji Wu

и другие.

Journal of Hazardous Materials, Год журнала: 2025, Номер unknown, С. 138260 - 138260

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0

Ferroptosis: Molecular perspective, cellular influence, cancer manifestation, and therapeutic potentials DOI
Pawan Kumar Pandey,

Saurabh Bhorkade,

Shikha Jha

и другие.

Journal of Drug Delivery Science and Technology, Год журнала: 2024, Номер 100, С. 105998 - 105998

Опубликована: Июль 31, 2024

Язык: Английский

Процитировано

2