Long non-coding RNA Neat1 triggers renal tubular epithelial cell apoptosis via activating BH3-only protein in membranous nephropathy.

Background And Objective: Membranous nephropathy (MN) is an autoimmune disease. The up-regulation of the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (Neat1) has been found in MN but the mechanism is still unclear. Here, we explored the effect and the underlying mechanism of lncRNA Neat1 on the apoptosis of renal tubular epithelial cells in MN.

Clinical characteristics of patients with uremia undergoing maintenance hemodialysis complicated with COVID-19.

This study aimed to evaluate the onset characteristics of patients with uremia undergoing maintenance hemodialysis complicated with COVID-19, so as to improve the understanding, diagnosis, and treatment.26 cases were confirmed cases of COVID-19. Confirmed patients with COVID-19 undergoing maintenance hemodialysis in the blood purification center were recruited.

Up-regulation of miR-135b expression induced by oxidative stress promotes the apoptosis of renal tubular epithelial cells under high glucose condition.

This study aimed to investigate the role and underlying mechanism of miR-135b in high glucose-induced oxidative stress of renal tubular epithelial cells. Here, in vivo experiments found that compared to the control group, miR-135b expression was significantly up-regulated in the diabetes group, whereas BMP7 mRNA and protein levels were down-regulated. In high glucose-treated renal tubular epithelial cells (HK-2) in vitro, oxidative stress was induced, which up-regulated miR-135b expression.

Sinomenine alleviates high glucose-induced renal glomerular endothelial hyperpermeability by inhibiting the activation of RhoA/ROCK signaling pathway.

As an early sign of diabetic cardiovascular disease, endothelial dysfunction may contribute to progressive diabetic nephropathy (DN). Endothelial hyperpermeability induced by hyperglycemia (HG) is a central pathogenesis for DN. Sinomenine (SIN) has strong anti-inflammatory and renal protective effects, following an unknown protective mechanism against HG-induced hyperpermeability.