Evidence map›Paper›PMID 32550152›Full record

ArticleJournal of diabetes and metabolic disorders2020

miR-29b attenuates histone deacetylase-4 mediated podocyte dysfunction and renal fibrosis in diabetic nephropathy.

Piyush Gondaliya, Aishwarya P Dasare, Kavya Jash, Rakesh Kumar Tekade, Akshay Srivastava, Kiran Kalia

Open access · greenAbstract read
In one paragraph

Article in Journal of diabetes and metabolic disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Advances in the Epigenetic Mechanisms of Diabetic Nephropathy Pathogenesis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
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  9. The anti-inflammatory activity of probioticJournal of diabetes and metabolic disorders · 2023
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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 at 1 institution in 1 country.

Piyush GondaliyaDepartment of Biotechnology, National Institute of Pharmaceutical Education and Research- Ahmedabad, opposite Air force station, Palaj, Gandhinagar, Gujarat 382355 India.
Aishwarya P DasareDepartment of Biotechnology, National Institute of Pharmaceutical Education and Research- Ahmedabad, opposite Air force station, Palaj, Gandhinagar, Gujarat 382355 India.
Kavya JashDepartment of Biotechnology, National Institute of Pharmaceutical Education and Research- Ahmedabad, opposite Air force station, Palaj, Gandhinagar, Gujarat 382355 India.
Rakesh Kumar TekadeDepartment of Pharmaceutics, National Institute of Pharmaceutical Education and Research- Ahmedabad, opposite Air force station, Palaj, Gandhinagar, Gujarat 382355 India.
Akshay SrivastavaDepartment of Medical Devices, National Institute of Pharmaceutical Education and Research- Ahmedabad, opposite Air force station, Palaj, Gandhinagar, Gujarat 382355 India.
Kiran KaliaDepartment of Biotechnology, National Institute of Pharmaceutical Education and Research- Ahmedabad, opposite Air force station, Palaj, Gandhinagar, Gujarat 382355 India.
National Institute of Pharmaceutical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAs epigenetic modifications like chromatin histone modifications have been suggested to play a role in the pathophysiology of Diabetic Nephropathy (DN) and are also found to be regulated by microRNAs. Our main purpose was to explore the role of microRNA in histone modulations associated with DN. There is downregulation of miR-29b due to advanced glycation end products in diabetes. Histone Deacetylase-4 (HDAC4) is amongst the histone modulators which promotes podocytes' impairment and upregulates transforming growth factor-1 (TGF-β1) leading to renal fibrosis. Moreover, macrophage infiltration causes podocytes' apoptosis and IL-6 mediated inflammation. As miR-29b is downregulated in diabetes and HDAC4, TGF-β1 and IL-6 could be the possible therapeutic targets in DN, our study was focussed on unveiling the role of miR-29b in modulation of HDAC4 and hence, in podocyte dysfunction and renal fibrosis in DN.

methodsIn silico analysis and luciferase assay were done to study the interaction between miR-29b and HDAC4. In-vitro DN model was developed in podocytes and miR-29b mimics were transfected

resultsIt was found that miR-29b targets the 3' untranslated region of HDAC4. In both in-vitro and in-vivo DN model, downregulation of miR-29b and subsequent increase in HDAC4 expression was observed. The miR-29b mimics suppressed podocytes' inflammation mediated through macrophages and attenuated HDAC4 expression, glomerular damage and renal fibrosis.

conclusionThis study concludes that miR-29b regulates the expression of HDAC4 which plays a role in controlling renal fibrosis and podocytes' impairment in DN.

Indexed as

Diabetic nephropathyHDAC4Histone modificationsmiR-29bRenal fibrosisTGF-β1

Identifiers

PMID32550152
PMCPMC7270417
OpenAlexW2995014118

What OpenQuestion holds

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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.