Evidence map›Paper›PMID 38863972›Full record

ArticleIET nanobiotechnology2024

Renal Tissue-Derived Exosomal miRNA-34a in Diabetic Nephropathy Induces Renal Tubular Cell Fibrosis by Promoting the Polarization of M1 Macrophages.

Shuai Zheng, Yi Zeng, Liqing Chu, Taiyang Gong, Sihong Li, Min Yang

Abstract read
In one paragraph

Article in IET nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. [Experimental investigation of skin tissue-derived extracellular vesicles isolated from type 2 diabetic foot ulcers in impaired wound healing].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026
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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

6 authors.

Shuai ZhengDepartment of Nephrology, The Second Affiliated Hospital, Kunming Medical University, No. 347 Dianmian Street, Kunming, Yunnan 650101, China.ORCID https://orcid.org/0000-0002-1742-7268
Yi ZengDepartment of Nephrology, The Second Affiliated Hospital, Kunming Medical University, No. 347 Dianmian Street, Kunming, Yunnan 650101, China.ORCID https://orcid.org/0000-0001-6380-5082
Liqing ChuDepartment of Nephrology, The Second Affiliated Hospital, Kunming Medical University, No. 347 Dianmian Street, Kunming, Yunnan 650101, China.
Taiyang GongDepartment of Nephrology, The Second Affiliated Hospital, Kunming Medical University, No. 347 Dianmian Street, Kunming, Yunnan 650101, China.ORCID https://orcid.org/0009-0001-4566-1596
Sihong LiDepartment of Nephrology, The Second Affiliated Hospital, Kunming Medical University, No. 347 Dianmian Street, Kunming, Yunnan 650101, China.ORCID https://orcid.org/0009-0007-6460-6465
Min YangDepartment of Nephrology, The Second Affiliated Hospital, Kunming Medical University, No. 347 Dianmian Street, Kunming, Yunnan 650101, China.ORCID https://orcid.org/0009-0002-8961-4254

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Diabetic nephropathy (DN) is the leading cause of chronic kidney disease, and the activation and infiltration of phagocytes are critical steps of DN. This study aimed to explore the mechanism of exosomes in macrophages and diabetes nephropathy and the role of miRNA-34a, which might provide a new path for treating DN. Materials and Methods: The DN model was established, and the success of the model establishment was confirmed by detecting general indicators, HE staining, and immunohistochemistry. Electron microscopy and NanoSight Tracking Analysis (NTA) were used to see the morphology and size of exosomes. MiRNA-34a inhibitor, miRNA-34a mimics, pc- Results: An animal model of diabetic nephropathy was successfully constructed. Macrophages could phagocytose exosomes. After ingesting model exosomes, M1 macrophages were activated, while M2 macrophages were weakened, indicating the model mice's kidney exosomes caused the polarization. MiRNA-34a inhibitor increased Conclusion: Exosomal miRNA-34a of tubular epithelial cells promoted M1 macrophage activation in diabetic nephropathy via negatively regulating

Indexed as

Diabetic NephropathiesExosomesFibrosisMacrophagesMicroRNAsAnimalsDiabetes Mellitus, ExperimentalDisease Models, AnimalKidney TubulesMaleMiceMice, Inbred C57BLMicroRNAsMIRN34a microRNA, mouse

Identifiers

PMID38863972
PMCPMC11095076

What Socratic holds

Textmetadata
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 Socratic graph.