Evidence map›Paper›PMID 41079928›Full record

ArticleInternational journal of biological sciences2025

HIF-1-mediated macrophage metabolic reprogramming promotes AKI to CKD transition.

Hong Ding, Yan Zhou, Ren-He Zhu, Shu Yu, Ai-Qing Zhang, Hong Liu, Jia-Ling Ji, Zuo-Lin Li

Abstract read
In one paragraph

Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026
    Review
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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

8 authors.

Hong DingInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.
Yan ZhouInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.
Ren-He ZhuInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.
Shu YuInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.
Ai-Qing ZhangDepartment of Pediatrics, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, P.R. China.
Hong LiuInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.
Jia-Ling JiDepartment of Pediatrics, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, P.R. China.
Zuo-Lin LiInstitute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage is educated by the tubule epithelial cell with maladaptive repair during the renal maladaptive repair, which is one of the most important characteristic features in acute kidney injury (AKI) to chronic kidney disease (CKD) transition. However, the underlying mechanism of orchestrating characterization of macrophage in renal maladaptive repair remains largely unclear. Accordingly, we found that pro-inflammatory macrophage educated by tubule epithelial cell with maladaptive repair was the primary contributor to the renal maladaptive repair in AKI to CKD transition, because macrophages depletion significantly attenuated tubulointerstitial fibrosis. Meanwhile, we found that glycolysis was essential for maintaining pro-inflammatory macrophage phenotype. Further, we demonstrated that HIF-1α played a crucial role in macrophage glycolysis as myeloid

Indexed as

Acute Kidney InjuryHypoxia-Inducible Factor 1, alpha SubunitMacrophagesRenal Insufficiency, ChronicAnimalsFibrosisGlycolysisMaleMetabolic ReprogrammingMiceMice, Inbred C57BLMice, KnockoutNF-kappa BHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitNF-kappa Bacute kidney injurychronic kidney diseasehypoxia-inducible factor-1macrophagemetabolic reprogrammingNF-κB

Identifiers

PMID41079928
PMCPMC12509917

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.