What question did this study set out to answer?

Assess the contribution of JNK3 to TGF-β-mediated glomerular fibrosis and injury in chronic kidney disease.

Selective JNK3 Inhibition Ameliorates TGF-β–Mediated Glomerular Injury and Fibrosis in the Kidneys

View Full Paper

Ask AI

Bookmark

Assess the contribution of JNK3 to TGF-β-mediated glomerular fibrosis and injury in chronic kidney disease.
Examined JNK3 expression in differentiated human podocytes and kidney cortex tissues from CKD patients.
Utilized an adriamycin-induced mouse model of glomerulosclerosis for in vivo analysis.
Employed genetic and pharmacologic interventions to inhibit JNK signaling in TGF-β responses.
Increased JNK3 expression and c-Jun phosphorylation were observed in CKD patients and adriamycin-treated mice.
JNK inhibition diminished TGF-β activation of Smad2/3 and ERK signaling, and reduced albumin permeability.
The selective JNK3 inhibitor JMH021 improved kidney dysfunction and fibrosis compared to the pan-JNK inhibitor SP600125.

No takes yet. Share an insight, caveat, or question.

Randomized trial demonstrates reduced kidney injury in CKD through selective JNK3 inhibition, suggesting a new treatment approach.

Choi et al. (2026) studied this question.

View Full Paper

Ask AI

Bookmark