Evidence map›Paper›PMID 40369631›Full record

ReviewDiabetology & metabolic syndrome2025

The status of studies on the mechanism of microcirculatory dysfunction in the process of diabetic kidney injury.

Zeng Wu, Yu Gao, Chun-Yue Zuo, Xiao-Rong Wang, Xiao-Han Chen, Xiao-Hong Zhou, Wei-Juan Gao

Abstract readReview
In one paragraph

Review in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
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

7 authors.

Zeng WuHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
Yu GaoHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
Chun-Yue ZuoHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
Xiao-Rong WangHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
Xiao-Han ChenHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
Xiao-Hong ZhouHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China. zxh19703@163.com.
Wei-Juan GaoHebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China. gwj6088@163.com.

Funding

Hebei Province Graduate Innovation Funding Project XCXZZBS2024001Major Special Project of National Natural Science Foundation of China 32141005
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is one of the most common and serious microvascular complications of diabetes mellitus (DM) and is the main cause of end-stage renal disease. Endothelial dysfunction caused by persistent hyperglycemia occurs at the initial stage of vascular disease. Moreover, persistent hyperglycemia is also a critical factor causing renal microcirculatory dysfunction. In recent years, many studies have confirmed that chronic hypoxia caused by microcirculatory dysfunction is one of the main mechanisms of kidney injury in patients with DM. Similarly, microcirculatory dysfunction damages renal tissue through interactions with other pathophysiological processes, thereby promoting the occurrence and development of DN. Thus, this article reviews the pathogenesis of renal microcirculatory dysfunction in DM and its interaction with stress, energy metabolism, and immunologic inflammation. Furthermore, a new idea was proposed to analyze the mechanism of kidney injury in DM from the perspective of microcirculatory dysfunction.

Indexed as

Diabetic nephropathyEndothelial dysfunctionInflammationMicrocirculationRenal hypoxia

Identifiers

PMID40369631
PMCPMC12076956

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.