Evidence map›Paper›PMID 30734599›Full record

ArticleJournal of enzyme inhibition and medicinal chemistry2019

A mitochondrial-targeted peptide ameliorated podocyte apoptosis through a HOCl-alb-enhanced and mitochondria-dependent signalling pathway in diabetic rats and in vitro.

Xiaoqiao Wang, Dongdong Tang, Yaowei Zou, Xiaoyu Wu, Yihua Chen, Hongying Li, Siqi Chen, Yue Shi, Hongxin Niu

Open access · goldAbstract read
In one paragraph

Article in Journal of enzyme inhibition and medicinal chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022
    Review
  12. Article
  13. TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. 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

9 authors at 2 institutions in 1 country.

Xiaoqiao Wanga Division of Nephrology, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Dongdong Tangb Division of Nephrology, Huadu District people's Hospital , Southern Medical University , Guangzhou , China.
Yaowei Zoua Division of Nephrology, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Xiaoyu Wua Division of Nephrology, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Yihua Chena Division of Nephrology, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Hongying Lic Special Medical Service Center, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Siqi Chena Division of Nephrology, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Yue Shic Special Medical Service Center, Zhujiang Hospital , Southern Medical University , Guangzhou , China.
Hongxin Niuc Special Medical Service Center, Zhujiang Hospital , Southern Medical University , Guangzhou , China.ORCID http://orcid.org/0000-0001-8187-7522
Zhujiang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria play important roles in the development of diabetic kidney disease (DKD). The SS peptide is a tetrapeptide that is located and accumulated in the inner mitochondrial membrane; it reduces reactive oxygen species (ROS) and prevents mitochondrial dysfunction. Podocytes are key cellular components in DKD progression. However, whether the SS peptide can exert renal protection through podocytes and the mechanism involved are unknown. In the present study, we explored the mechanisms of the SS peptide on podocyte injury in vivo and in vitro. Compared with the control group, the glomerular podocyte number and expression of WT1 were significantly reduced and TUNEL-positive podocytes were significantly increased in renal tissues in the diabetic rat. These effects were further exacerbated by hypochlorite-modified albumin (HOCl-alb) challenge but prevented by SS-31. In vitro, SS-31 blocked apoptosis in podocyte cell line induced by HOCl-alb. SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases. These data suggest that SS-31 may prevent podocyte apoptosis, exerting renal protection in diabetes mellitus, probably through an apoptosis-related signalling pathway involving oxidative stress and culminating in mitochondria.

Indexed as

AnimalsApoptosisDiabetes Mellitus, ExperimentalDose-Response Relationship, DrugHypochlorous AcidMaleMitochondriaMolecular StructurePodocytesRatsRats, Sprague-DawleySerum AlbuminSignal TransductionStructure-Activity RelationshipHypochlorous AcidSerum Albuminantioxidant peptidediabetic kidney diseasehypochlorite-modified albuminmitochondriaPodocyte apoptosis

Identifiers

PMID30734599
PMCPMC6327984
OpenAlexW2910515662

What OpenQuestion holds

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LicenceCC BY-NC
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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.