HBx promotes podocyte-macrophage transdifferentiation by mediating NLRP3 expression in hepatitis B virus-associated glomerulonephritis.

ABSTRACT:

Background

Podocytes are identified as main injury targets in the pathogenesis of hepatitis B virus (HBV)-associated glomerulonephritis (HBV-GN). NLR family pyrin domain containing 3 (NLRP3) has a critical function in ​inducing podocyte injury across multiple renal pathologies. This study aimed to explore whether NLRP3 expression linked to podocyte injury participated in the pathogenic mechanism of HBV-GN.

Methods

The expression of NLRP3, CD68, ‌intercellular cell adhesion molecule-1 (‌ICAM-1), and α-smooth muscle actin (α-SMA) was identified in HBV-GN renal biopsies. The correlations between renal NLRP3 expression and clinical parameters, as well as between HBV X (HBx) expression and inflammation and fibrosis markers, were analyzed. HBx-encoding plasmids were transferred in

SUBMITTER: He Z 

PROVIDER: S-EPMC12465676 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature