Aldosterone (Aldo) is an independent risk factor for chronic kidney disease (CKD), and
although Aldo directly induces renal tubular cell injury, the underlying mechanisms remain …

Growing evidence has shown that NLRP3 inflammasome activation promotes the
development of tubulointerstitial inflammation and progression of renal injury. We previously …

Abstract Background/Aims: Growing evidence suggests mitochondrial dysfunction (MtD) and
the Nlrp3 inflammasome play critical roles in chronic kidney disease (CKD) progression. We …

Aldosterone (Aldo) has been shown as an important contributor of podocyte injury. However,
the underlying molecular mechanisms are still elusive. Recently, the pathogenic role of NOD …

Background Reactive oxygen species (ROS) and inflammation both contribute to the
progression of aldosterone-induced renal injury. To better understand the underlying …

The NOD-like receptor family, pyrin domain containing-3 (NLRP3) inflammasome has been
implicated in renal inflammation and fibrosis. However, the biological function of …

Background: We previously reported that the NLRP3 inflammasome played an important
role in mediating the podocyte injury induced by aldosterone. However, more studies on the …

The NLRP3 inflammasome is activated by mitochondrial damage and contributes to kidney
fibrosis. However, it is unknown whether PGC-1α, a key mitochondrial biogenesis regulator …

Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and
chronic kidney disease. NLRX1 is a receptor of the innate immune system that is …

Background: Inflammation is a key feature of aldosterone-induced vascular damage and
dysfunction, but molecular mechanisms by which aldosterone triggers inflammation remain …