Results 131 to 140 of about 45,966 (272)

Isorhamnetin Alleviates Renal Fibrosis Induced by Renal Tubular Epithelial Cell Senescence Via Inhibition of the IL‐6/IL‐6R Signaling Pathway

open access: yesiMetaMed, EarlyView.
IL‐6 from RTECs upregulates TGF‐β in macrophages, promoting fibroblast transdifferentiation. Isorhamnetin inhibits this effect. ABSTRACT Chronic kidney disease (CKD) is a major global health issue. Kidney fibrosis is a key mechanism leading to end‐stage renal disease.
Weifei Liang   +8 more
wiley   +1 more source

Misdiagnosis of familial Mediterranean fever in patients with Anderson-Fabry disease [PDF]

open access: yes, 2013
Fabry disease (FD) is an underdiagnosed pathology due to its symptomatology that overlaps with various systemic and rheumatic disorders, including familial Mediterranean fever (FMF).
A.l.b.e.g.g.i.a.n.i. G   +8 more
core  

Oat β‐Glucan and Galactooligosaccharides Influence Gallstone Formation by Modulating the Gut Microbiota, Particularly Desulfovibrionales

open access: yesiMetaMed, EarlyView.
Oat β‐glucan and galactooligosaccharides influence the formation of gallstones by modulating the gut microbiota, particularly the abundance of Desulfovibrionales. The primary mechanism involves metabolic byproducts associated with Desulfovibrionales inhibiting hepatic bile acid synthesis via both the hepatic FXR–SHP and intestinal FXR–FGF15 signaling ...
Liang Tian   +20 more
wiley   +1 more source

Renal outcomes of agalsidase beta treatment for Fabry disease: role of proteinuria and timing of treatment initiation [PDF]

open access: yes, 2017
Background. The purpose of this study was to identify determinants of renal disease progression in adults with Fabry disease during treatment with agalsidase beta. Methods.
Beitner-Johnson, Dana   +15 more
core  

Targeting Microbiome Metabolites: Reshaping Immunotherapy and Clinical Management Strategies for Colorectal Cancer

open access: yesiMetaMed, EarlyView.
The occurrence and progression of colorectal cancer are intricately linked to metabolites produced by the gut microbiota. Metabolites generated by pathogenic microbial communities can promote colorectal cancer development by reshaping the immune microenvironment.
Xinrui Yang   +3 more
wiley   +1 more source

Dietary α-galactosidase and xylanase to improve the nutritional value of corn-soybean-rapeseed meal diets in broiler chickens

open access: yesJournal of Applied Animal Research
Two experiments were performed to assess the effects of an enzyme preparation (containing α-galactosidase and xylanase) on chicken performance, carcass traits, footpad dermatitis score, and nutrient digestibility.
Alberto Viñado   +5 more
doaj   +1 more source

Ginsenoside Rb1 Targets the HRD1‐STING Axis to Mitigate Cholesterol‐Induced VSMC Senescence

open access: yesJournal of Clinical Laboratory Analysis, EarlyView.
Schematic representation of the proposed mechanism of action for Ginsenoside Rb1. Suppression of HRD1 expression in VSMCs cholesterol stimulation, leading to ER stress (BiP/XBP1s upregulation), STING pathway activation, ROS accumulation (including mitochondrial ROS), and ultimately, VSMC senescence.
Haiming Niu   +5 more
wiley   +1 more source

Heart failure in two male patients with late‐onset Fabry mutation (IVS4 + 919G > A)

open access: yes
ESC Heart Failure, Volume 12, Issue 2, Page 1508-1513, April 2025.
Xufei Yang   +3 more
wiley   +1 more source

Loganin, an Iridoid Glycoside, Alleviates Paclitaxel‐Induced Skeletal Muscle Toxicity by Enhancing Mitochondrial Function, Boosting Antioxidant Defenses, and Reducing Cellular Senescence

open access: yesThe Kaohsiung Journal of Medical Sciences, EarlyView.
ABSTRACT Mitochondrial dysfunction and energy imbalance caused by chemotherapy are key contributors to skeletal muscle atrophy, which severely impacts the quality of life in cancer patients. Paclitaxel, a commonly used chemotherapeutic agent, is known to promote muscle wasting and cellular senescence, largely by impairing mitochondrial function.
Yu‐Fan Chuang   +6 more
wiley   +1 more source

Home - About - Disclaimer - Privacy