Calcitriol Treatment Attenuates Uric Acid-Induced Kidney Injury via Super Oxide Dismutase-1 (SOD-1) Upregulation and Fibrosis Reduction.

Background: Hyperuricemia induces nephropathy through the mediation of oxidative stress, tubular injury, inflammation, and fibrosis. The high uric acid level is associated with the reduction of vitamin D levels. However, the reno-protective effects of this vitamin in hyperuricemia condition remain unknown.

Vitamin D Ameliorates Kidney Ischemia Reperfusion Injury via Reduction of Inflammation and Myofibroblast Expansion.

The incidence rate of Acute Kidney Injury (AKI) gets escalated each year. Kidney ischemia/reperfusion injury (IR injury) is the main cause of AKI after major cardiovascular surgery, trauma, or kidney transplantation. Reperfusion is considered essential for ischemic tissue.

(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.

Heparanase upregulation from adipocyte associates with inflammation and endothelial injury in diabetic condition.

Background: Diabetes Mellitus (DM) is one of the metabolic diseases which leads to fatty tissue injury, and consequently inducing lipotoxicity and cellular senescence. This condition contributes to endothelial dysfunction with chronic inflammation and organ damage. Heparanase which has a role in disrupting endothelial surface layer (glycocalyx) may promote endothelial Nitric oxide synthase (eNOS) reduction and inflammation.

Ethanol Extract of (Gotu Kola) Attenuates Tubular Injury Through Inhibition of Inflammatory Cytokines and Enhancement of Anti-Fibrotic Factor in Mice with 5/6 Subtotal Nephrectomy.

Background: Chronic kidney disease (CKD) leads to inflammation, fibrosis and destruction of the renal architecture. (CeA) is an herbaceous plant with anti-inflammatory effects. We aimed to elucidate the effect of CeA on inflammation, fibrosis, vascular remodelling and antifibrotic substances in a 5/6 subtotal nephrectomy (SN) model in mice.

Chlorogenic Acid Attenuates Kidney Ischemic/Reperfusion Injury via Reducing Inflammation, Tubular Injury, and Myofibroblast Formation.

Kidney ischemic/reperfusion (I/R) injury is the main cause of acute kidney injury (AKI) involving renal function deterioration, renal architecture damage, and inflammation. This condition may lead to kidney fibrosis with epithelial to mesenchymal transition (EMT) and myofibroblast formation. Inhibition of chronic effects of kidney I/R injury may provide effective strategies for treating AKI and chronic kidney diseases (CKDs).

Reduction of Serum Uric Acid Associated with Attenuation of Renal Injury, Inflammation and Macrophages M1/M2 Ratio in Hyperuricemic Mice Model.

Background: Hyperuricemia contributed to endothelial dysfunction, activation of the RAS system, increased oxidative stress and maladaptive immune system response. M1 and M2 macrophages were known to contribute to the onset of renal fibrosis. This study aimed to look at the effect of lowering serum uric acid levels on renal injury in mice.

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.

Histochemical and Immunohistochemical Study of α-SMA, Collagen, and PCNA in Epithelial Ovarian Neoplasm.

Background: Alpha-smooth muscle actin (α-SMA) is an isoform of actin, positive in myofibroblasts and is an epithelial to mesenchymal transition (EMT) marker. EMT is a process by which tumor cells develop to be more hostile and able to metastasize. Progression of tumor cells is always followed by cell composition and extracellular matrix component alteration.

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.