Macula Densa Alleviates Shiga Toxin-Induced Acute Kidney Injury via CCN1-Mediated Renal Tubular Repair.

ABSTRACT: Shiga toxins (Stx), produced by Shiga toxin-producing Escherichia coli, preferentially attack renal tissue and frequently induce acute kidney injury (AKI) and renal failure. To prevent irreversible damage, the injured renal tissue, particularly renal tubular epithelium, mounts a remodeling and regeneration response to repair itself. However, how such intrinsic renal repair processes are initiated and coordinated in infected renal tubular regions remains elusive. Herein, we reported that macula densa apparatus, in addition to its conventional role as a salt sensor in nephron, can function as an endogenous sensor for exogenous toxins (e.g., Stx). We demonstrated that macula densa cells orchestrate a rapid repair niche by initiating transcriptional activation of repair and regeneration

SUBMITTER: Wan H 

PROVIDER: S-EPMC12474279 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature