Uric acid induces liver fibrosis through activation of inflammatory mediators and proliferating hepatic stellate cell in mice.

Introduction: Uric acid is associated with cardiometabolic risk factor and severity of liver damage. The mechanism of uric acid inducing liver damage is still elusive. This study elucidates the development of liver fibrosis under hyperuricemia.

(Gotu kola) ethanol extract up-regulates hippocampal brain-derived neurotrophic factor (BDNF), tyrosine kinase B (TrkB) and extracellular signal-regulated protein kinase 1/2 (ERK1/2) signaling in chronic electrical stress model in rats.

Objectives: Impairment of hippocampus function as a center for memory processing occurs due to stress. L. (Gotu kola) is known to improve memory, intelligence, and neural protection although the precise mechanism is not well understood.

Hyperuricemia Induces Wnt5a/Ror2 Gene Expression, Epithelial-Mesenchymal Transition, and Kidney Tubular Injury in Mice.

Background: Hyperuricemia contributes to kidney injury, characterized by tubular injury with epithelial-mesenchymal transition (EMT). Wnt5a/Ror2 signaling drives EMT in many kidney pathologies. This study sought to evaluate the involvement of Wnt5a/Ror2 in hyperuricemia-induced EMT in kidney tubular injury.

Uric acid causes kidney injury through inducing fibroblast expansion, Endothelin-1 expression, and inflammation.

Background: Uric acid (UA) plays important roles in inducing renal inflammation, intra-renal vasoconstriction and renal damage. Endothelin-1 (ET-1) is a well-known profibrotic factor in the kidney and is associated with fibroblast expansion. We examined the role of hyperuricemia conditions in causing elevation of ET-1 expression and kidney injury.

Vitamin D Attenuates Kidney Fibrosis via Reducing Fibroblast Expansion, Inflammation, and Epithelial Cell Apoptosis.

Kidney fibrosis is the common final pathway of chronic kidney diseases (CKD). It is characterized by myofibroblast formation, inflammation, and epithelial architecture damage. Vitamin D is known as a renoprotective agent, although the precise mechanism is not well understood.