Evidence map›Paper›PMID 36934129›Full record

ArticleScientific reports2023

Urinary exosomal miRNA-663a shows variable expression in diabetic kidney disease patients with or without proteinuria.

Nisha Sinha, Veena Puri, Vivek Kumar, Ritambhra Nada, Ashu Rastogi, Vivekanand Jha, Sanjeev Puri

Open access · goldFull text read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Urinary biomarkers of diabetic kidney disease.World journal of diabetes · 2026
    Review
  6. Research progress on the regulation of miRNAs in diabetic kidney disease and osteoporosis.International journal of clinical and experimental pathology · 2026
    Review
  7. Review
  8. Research progress on small extracellular vesicles in diabetic nephropathy.Frontiers in cell and developmental biology · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. 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 at 3 institutions in 1 country.

Nisha SinhaCentre for Stem Cell Tissue Engineering and Biomedical Excellence, Panjab University, Chandigarh, India.
Veena PuriCentre for Systems Biology and Bioinformatics, Panjab University, Chandigarh, India.
Vivek KumarDepartment of Nephrology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Ritambhra NadaDepartment of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Ashu RastogiDepartment of Endocrinology and Metabolism, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Vivekanand JhaThe George Institute for Global Health, New Delhi, India. vjha@georgeinstitute.org.in.
Sanjeev PuriDepartment of Biotechnology, University Institute of Engineering and Technology (UIET), Panjab University, Chandigarh, India. s_puri@pu.ac.in.
Post Graduate Institute of Medical Education and Research · INPanjab University · INGeorge Institute for Global Health · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterogeneity in the Diabetic Kidney Disease (DKD) diagnosis makes its rational therapeutics challenging. Although albuminuria characterizes DKD, reports also indicate its prevalence among non-proteinuric. Recent understanding of disease progression has thus inclined the focus on proximal tubular cell damage besides the glomeruli. A non-invasive approach exploiting exosomal miRNA derived from human kidney proximal tubular cell line was, hence, targeted. Upon miRNA profiling, three miRNAs, namely, hsa-miR-155-5p, hsa-miR-28-3p, and hsa-miR-425-5p were found to be significantly upregulated, while hsa-miR-663a was downregulated under diabetic conditions. Among these, hsa-miR-663a downregulation was more pronounced in non-proteinuric than proteinuric DKD subjects and was thus selected for the bioinformatics study. Ingenuity Pathway Analysis (IPA) narrowed on to IL-8 signaling and inflammatory response as the most enriched 'canonical pathway' and 'disease pathway' respectively, during DKD. Further, the putative gene network generated from these enriched pathways revealed experimentally induced diabetes, renal tubular injury, and decreased levels of albumin as part of mapping under 'disease and function'. Genes target predictions and annotations by IPA reiterated miR-663a's role in the pathogenesis of DKD following tubular injury. Overall, the observations might offer an indirect reflection of the underlying mechanism between patients who develop proteinuria and non-proteinuria.

Indexed as

Diabetes MellitusDiabetic NephropathiesMicroRNAsCell LineHumansKidneySignal TransductionMicroRNAsMIRN633 microRNA, human

Identifiers

PMID36934129
PMCPMC10024703
OpenAlexW4327813470

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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.