Endothelial Cell Dysfunction: Onset, Progression, and Consequences.

Endothelial cell dysfunction is a complex process involving various causes, early and late events, and subsequent consequences. This review provides an overview of each aspect and outlines therapeutic interventions targeting these stages. Causes of endothelial dysfunction encompass a spectrum of risk factors including hypertension, diabetes, smoking, obesity, inflammation, oxidative stress, and genetic predispositions.

Accelerated Senescence and Apoptosis in the Rat Liver during the Progression of Diabetic Complications.

Background: Chronic hyperglycaemia of diabetes causes long-term damage and impaired function of multiple organs. However, the pathological changes in the liver following long-term diabetes remain unclear. This study aimed to determine the pathological complications of long-term diabetes in the rat liver.

Calcitriol attenuates vascular remodeling in association with alteration of ppET-1/ETR/eNOS and ETR expression in acute and chronic phases of kidney ischemia-reperfusion injury in mice.

Kidney ischemia-reperfusion injury (IRI) causes acute kidney injury with increasing risk of maladaptive repair through endothelin-1 (ET-1)/endothelin type A receptor (ETR) signaling. Calcitriol shows renoprotection in kidney fibrosis, however, its effects on vasoactive substances expression and vascular remodeling following kidney IRI remain unclear. This research aimed to investigate Calcitriol's effects on preproendothelin-1 (), , endothelial nitric oxide synthase () mRNA expression and vascular remodeling in acute and chronic phases of kidney IRI in mice.

Ethanolic Extract of Treatment in the Early Stage of Hyperglycemia Condition Inhibits Glomerular Injury and Vascular Remodeling in Diabetic Rat Model.

Background: Diabetes mellitus (DM) is marked by oxidative stress, inflammation, and vascular dysfunction that caused diabetic nephropathy that resulted in end-stage renal disease (ESRD). Vascular dysfunction is characterized by an imbalance in vasoconstrictor and vasodilator agents which underlies the mechanism of vascular injury in DM. Additionally, diminished podocytes correlate with the severity of kidney injury.

Extract Attenuates Kidney Fibrosis Through Reducing Mesenchymal Transition and Inflammation in Ureteral Ligation Model in Mice.

Kidney fibrosis is the common final pathway of chronic kidney disease (CKD) and is characterized by inflammation, mesenchymal transition with myofibroblast formation and epithelial to mesenchymal transition (EMT). (CeA) is an herb that has a reno-protective effect. However, its mechanism of action in kidney fibrosis has not been elucidated.

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.

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.