KLF4 in Macrophages Attenuates TNFα-Mediated Kidney Injury and Fibrosis.

ABSTRACT:

Background

Polarized macrophage populations can orchestrate both inflammation of the kidney and tissue repair during CKD. Proinflammatory M1 macrophages initiate kidney injury, but mechanisms through which persistent M1-dependent kidney damage culminates in fibrosis require elucidation. Krüppel-like factor 4 (KLF4), a zinc-finger transcription factor that suppresses inflammatory signals, is an essential regulator of macrophage polarization in adipose tissues, but the effect of myeloid KLF4 on CKD progression is unknown.

Methods

We used conditional mutant mice lacking KLF4 or TNFα (KLF4's downstream effector) selectively in myeloid cells to investigate macrophage KLF4's role in modulating CKD progression in two models of CKD that feature robust macrophage accumulation,

SUBMITTER: Wen Y 

PROVIDER: S-EPMC6779357 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature