Evidence map›Paper›PMID 39119903›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Identification of a Novel ECM Remodeling Macrophage Subset in AKI to CKD Transition by Integrative Spatial and Single-Cell Analysis.

Yi-Lin Zhang, Tao-Tao Tang, Bin Wang, Yi Wen, Ye Feng, Qing Yin, Wei Jiang, Yue Zhang, Zuo-Lin Li, Min Wu and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed.

  1. Article
  2. Article
  3. Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026
    Review
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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Yi-Lin ZhangInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Tao-Tao TangInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Bin WangInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Yi WenInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Ye FengInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Qing YinInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Wei JiangInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Yue ZhangInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Zuo-Lin LiInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Min WuInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Qiu-Li WuInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Jing SongInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Steven D CrowleyDivision of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, NC, 27705, USA.
Hui-Yao LanDepartments of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, and Lui Che Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Hong Kong, 999077, China.
Lin-Li LvInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.
Bi-Cheng LiuInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, 210009, China.ORCID 0000-0002-4584-1853

Funding

National Key Research and Development Program of China 2022YFC2502500National Natural Science Foundation of China 81720108007National Natural Science Foundation of China 82030024National Natural Science Foundation of China 82122011National Natural Science Foundation of China 82200772National Natural Science Foundation of China 82230022National Natural Science Foundation of China 82241045Natural Science Foundation of Jiangsu Province BK20220828
6 · The paper itself

Abstract

The transition from acute kidney injury (AKI) to chronic kidney disease (CKD) is a critical clinical issue. Although previous studies have suggested macrophages as a key player in promoting inflammation and fibrosis during this transition, the heterogeneity and dynamic characterization of macrophages are still poorly understood. Here, we used integrated single-cell RNA sequencing and spatial transcriptomic to characterize the spatiotemporal heterogeneity of macrophages in murine AKI-to-CKD model of unilateral ischemia-reperfusion injury. A marked increase in macrophage infiltration at day 1 was followed by a second peak at day 14 post AKI. Spatiotemporal profiling revealed that injured tubules and macrophages co-localized early after AKI, whereas in late chronic stages had spatial proximity to fibroblasts. Further pseudotime analysis revealed two distinct lineages of macrophages in this transition: renal resident macrophages differentiated into the pro-repair subsets, whereas infiltrating monocyte-derived macrophages contributed to chronic inflammation and fibrosis. A novel macrophage subset, extracellular matrix remodeling-associated macrophages (EAMs) originating from monocytes, linked to renal fibrogenesis and communicated with fibroblasts via insulin-like growth factors (IGF) signalling. In sum, our study identified the spatiotemporal dynamics of macrophage heterogeneity with a unique subset of EAMs in AKI-to-CKD transition, which could be a potential therapeutic target for preventing CKD development.

Indexed as

Acute Kidney InjuryDisease Models, AnimalExtracellular MatrixMacrophagesRenal Insufficiency, ChronicSingle-Cell AnalysisAnimalsDisease ProgressionFibrosisMaleMiceMice, Inbred C57BLAKICKDmacrophagesingle‐cell RNA‐seqspatial transcriptomic

Identifiers

PMID39119903
PMCPMC11481374

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.