Evidence map›Paper›PMID 31571956›Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2019

Calpain-10 drives podocyte apoptosis and renal injury in diabetic nephropathy.

Tao Wang, Yanbin Gao, Xiaolei Wang, Yimin Shi, Jiayi Xu, Bingjie Wu, Jiaxin He, Yimeng Li

Open access · goldAbstract read
In one paragraph

Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2019. 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
1.6field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
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  7. Review
  8. Article
  9. Long non-coding RNAExperimental and therapeutic medicine · 2020
    Article
  10. Article
  11. Ginsenoside Rg1 Alleviates Podocyte Injury Induced by Hyperlipidemia via Targeting the mTOR/NF-Evidence-based complementary and alternative medicine : eCAM · 2020
    Article
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

8 authors at 1 institution in 1 country.

Tao WangSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.
Yanbin GaoSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-9547-5652
Xiaolei WangSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.
Yimin ShiSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.
Jiayi XuSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.
Bingjie WuSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.
Jiaxin HeSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, People's Republic of China.
Yimeng LiBeijing Key Laboratory of TCM Collateral Disease Theory Research, Beijing, People's Republic of China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is a progressive microvascular complication of diabetes mellitus (DM), driven largely by podocyte apoptosis. The cysteine protease Calpain 10 is known to augment apoptosis and necrosis, and is a potential therapeutic target in DN.

methodsType 2 diabetes was induced in SD rats by high-fat diet (HFD) feeding and streptozotocin (STZ) injections, and simulated in vitro by culturing conditionally immortalized mouse podocytes in hyperlipidemic (PA, 100 μM) conditions. The rate of apoptosis in the renal tissues and cultured podocytes was determined by TUNEL assay. The expression of Calpain 10 and its biological effects were assayed by real-time PCR, Western blotting, immunofluorescence and electron microscopy.

resultsCalpain 10 was up-regulated in the kidneys of DN rats, as well as immortalized mouse podocytes. High levels of Calpain 10 was associated with renal dysfunction and tissue destruction, and podocyte injury and apoptosis. Knockdown of Calpain 10 protected podocytes by decreasing apoptosis rate, and upregulated nephrin.

conclusionCalpain 10 is a pro-apoptotic factor in DN, and can be targeted for treating glomerular diseases.

Indexed as

apoptosisCalpain 10diabetic nephropathypodocyte

Identifiers

PMID31571956
PMCPMC6750010
OpenAlexW2972335684

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.