ArticleCell death & disease2025
Tubule-derived CCN1 drives renal repair via α
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- D4F-Functionalized Ceria Nanozyme-CasRx Platform Suppresses STING and Reprograms the Renal Immune Niche in Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Kindlins in the cardiovascular system: from development to pathogenesis.Frontiers in cardiovascular medicine · 2026Review
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Authors and funding
14 authors.
Funding
Abstract
Macrophages play a critical role in injury and repair following acute kidney injury (AKI), but their regulatory mechanisms remain incompletely understood. Cellular communication network factor 1 (CCN1), a secreted matricellular protein and early biomarker of AKI, may regulate macrophage function during kidney injury. In this study, we first investigated CCN1's interaction with macrophages in a murine model of ischemia-reperfusion (I/R)-induced AKI. The role of CCN1 was further investigated using recombinant protein administration, a renal tubular epithelial cell (RTEC)-specific CCN1 knockdown mouse model via adeno-associated virus, and in vitro studies with bone marrow-derived macrophages (BMDMs). We found that in response to injury, RTECs upregulated and secreted CCN1, which colocalized with infiltrating F4/80
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