Evidence map›Paper›PMID 31349216›Full record

ArticleEndocrine connections2019

Increased mitochondrial fission of glomerular podocytes in diabetic nephropathy.

Yiqiong Ma, Zhaowei Chen, Yu Tao, Jili Zhu, Hongxia Yang, Wei Liang, Guohua Ding

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  10. Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024
    Review
  11. C5a-C5aR1 axis controls mitochondrial fission to promote podocyte injury in lupus nephritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
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  14. Store-operated CaAmerican journal of physiology. Renal physiology · 2023
    Article
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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

7 authors at 2 institutions in 1 country.

Yiqiong MaDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Zhaowei ChenDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Yu TaoDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Jili ZhuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Hongxia YangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Wei LiangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Guohua DingDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsPrevious studies showed that abnormal mitochondrial structure and function were involved in the pathological process of diabetic nephropathy (DN). The dynamic mitochondrial processes, including fusion and fission, maintain the mass and quantity of mitochondria. Podocyte injury is a critical factor in the development and progression of DN. The present study evaluated the mitochondrial fission of podocytes in patients with DN.

methodsWe recruited 31 patients with biopsy-confirmed DN. A quantitative analysis of the mitochondrial morphology was conducted with electron microscopy using a computer-assisted morphometric analysis application to calculate the aspect ratio values. Immunofluorescence assays were used to evaluate protein colocalization in the glomeruli of patients.

resultsThe urine protein level was significantly increased in DN patients compared to non-DN patients (P < 0.001), and the mitochondria in the podocytes from DN patients were more fragmentated than those from patients without DN. The mitochondrial aspect ratio values were negatively correlated with the proteinuria levels (r = -0.574, P = 0.01), and multiple regression analysis verified that the mitochondrial aspect ratio was significantly and independently associated with the urine protein level (β = -0.519, P = 0.007). In addition, Drp1, a mitochondrial fission factor, preferentially combines with AKAP1, which is located in the mitochondrial membrane.

conclusionsIn the podocytes of DN patients, mitochondrial fragmentation was increased, and mitochondrial aspect ratio values were correlated with the proteinuria levels. The AKAP1-Drp1 pathway may contribute to mitochondrial fission in the pathogenesis of DN.

Indexed as

diabetesmetabolism

Identifiers

PMID31349216
PMCPMC6709540
OpenAlexW2965173707

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.