Evidence map›Paper›PMID 32727744›Full record

ArticleBMJ open diabetes research & care2020

miR-196b-5p-enriched extracellular vesicles from tubular epithelial cells mediated aldosterone-induced renal fibrosis in mice with diabetes.

Renzhi Hu, Xuan Li, Chuan Peng, Ruifei Gao, Linqiang Ma, Jinbo Hu, Ting Luo, Hua Qing, Yue Wang, Qian Ge and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMJ open diabetes research & care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% of its field
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023
    Review
  18. Review
  19. Article
  20. 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

17 authors at 4 institutions in 3 countries.

Renzhi Hu *Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xuan Li *Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0003-2202-0080
Chuan Peng *The Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ruifei GaoSchool of Public Health and Management, Chongqing Medical University, Chongqing, China.
Linqiang MaDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jinbo HuDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ting LuoDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hua QingDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yue WangDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qian GeDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Zhihong WangDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0003-3196-1739
Chaodong WuNutrition & Food Sciences, Texas A&M University, College Station, Texas, USA.ORCID 0000-0001-8569-8070
Xiaoqiu XiaoThe Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jun YangCentre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Morag J YoungCentre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Qifu LiDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China liqifu@yeah.net 443068494@qq.com.ORCID 0000-0001-7249-6445
Shumin YangDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China liqifu@yeah.net 443068494@qq.com.
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNHudson Institute of Medical Research · AUChongqing Public Health Medical Center · CNTexas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAldosterone is a mediator of progressive renal disease, but the mechanisms for aldosterone-mediated renal impairment in mice with diabetes are not fully defined.

methodsAldosterone and/or mineralocorticoid receptor antagonist eplerenone were used to treat the db/db mice with diabetes. Proximal tubule epithelial cells (PTECs) and fibroblasts were cultured. Blood and kidney samples from patients with diabetes with or without diabetic kidney disease (DKD) were used to verify the findings from animals and cultured cells.

resultsWe found that aldosterone promoted proteinuria and tubulointerstitial extracellular matrix (ECM) accumulation in db/db mice with diabetes while eplerenone mitigated the adverse effect of aldosterone. However, coculture of PTECs and fibroblasts found that when PTECs-derived extracellular vesicles (EVs) were taken up by fibroblasts, ECM production increased remarkably. Moreover, C57BL/6 mice injected with EVs from renal cortex of aldosterone-treated db/db mice showed increased ECM accumulation. Function of the ingredients of PTECs-derived EVs were analyzed, and RNAs were identified to be responsible for the EVs-induced fibroblast dysfunction. Furthermore, microRNA (miRNA) array analysis revealed that miR-196b-5p was the most remarkably increased miRNA in PTECs-derived EVs with aldosterone stimulation. Overexpression of miR-196b-5p in fibroblasts increased ECM production, accompanied by inhibition of the SOCS2 expression and enhanced STAT3 phosphorylation. In addition, plasma levels of miR-196b-5p was higher in patients with DKD as compared with patients without DKD and miR-196b-5p levels positively correlated with the albuminuria concentration. In kidney specimens from patients with diabetes, expression of miR-196b-5p, located mainly in PTECs, increased in patients with DKD as compared with the non-DKD.

conclusionThis study demonstrates the involvement of miR-196b-5p-EVs pathway as a novel mechanism in aldosterone-induced renal fibrosis in diabetes. EVs rich in miR-196b-5p mediate the crosstalk between PTECs and fibroblast during the development of renal fibrosis, which might be associated with STAT3/SOCO2 signaling pathway.

Indexed as

Diabetes MellitusDiabetic NephropathiesExtracellular VesiclesMicroRNAsAldosteroneAnimalsEpithelial CellsFibrosisHumansMiceMice, Inbred C57BLAldosteroneMicroRNAsMIRN196 microRNA, humanMIRN196 microRNA, mousefibroblastfibrosistubulointerstitial changes

Identifiers

PMID32727744
PMCPMC7394302
OpenAlexW3045858020

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.