Macrophage fate decisions during AKI-CKD transition insights from single-cell and spatial transcriptomics

Clicks: 14
ID: 332157
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #140 of 150 articles by views in nephrology dialysis transplantation

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 150 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Acute kidney injury (AKI) is an established risk factor for chronic kidney disease (CKD), but the cellular events that determine recovery or maladaptive repair remain incompletely defined. Macrophages are central regulators of this transition because their functional states change with time and tissue context. Recent single-cell RNA sequencing and spatial transcriptomic studies show that renal macrophages cannot be adequately described by a simple M1/M2 scheme. Instead, inflammatory, cycling, reparative and profibrotic programs emerge in a model- and niche-dependent manner. Experimental studies identify early S100A8/A9-associated inflammatory macrophages, cycling states and repair-associated programs involving TREM2, MRC1/IGF1 and efferocytosis. Together, these changes define a transient reparative phase in which inflammation can resolve and tubular repair can proceed. Failure to sustain this phase is associated with persistent inflammation, fibro-inflammatory niches, CD38-high and scar-associated macrophages, and progression towards fibrosis. Spatial transcriptomics further shows that interactions with injured tubular cells, fibroblasts, endothelial cells, immune cells and platelets shape macrophage function. Although the timing and dominant populations differ across experimental models, several pathway-level programs recur. Human datasets support selected inflammatory and fibrotic macrophage states but show limited one-to-one conservation of cell subsets across species. Clinical translation will therefore require conserved macrophage programs, treatment windows and biomarkers that distinguish reparative from maladaptive responses.
Reference Key
openalex_W7221566472 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Zhuo Feng, X. Li, Zixia Li, Xiang Yan, Jia Wei
Are you one of these authors? Claim your profile
Journal nephrology dialysis transplantation
Year 2026
DOI
10.1093/ndt/gfag236
URL
https://doi.org/10.1093/ndt/gfag236
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.