Evidence map›Paper›PMID 31281569›Full record

ArticleOxidative medicine and cellular longevity2019

Mitochondria-Targeted Peptide SS31 Attenuates Renal Tubulointerstitial Injury via Inhibiting Mitochondrial Fission in Diabetic Mice.

Shi-Kun Yang, Ai-Mei Li, Ya-Chun Han, Can-Hui Peng, Na Song, Ming Yang, Ming Zhan, Ling-Feng Zeng, Pan-Ai Song, Wei Zhang and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

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  20. SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022
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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

12 authors at 2 institutions in 1 country.

Shi-Kun YangDepartment of Nephrology, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.ORCID 0000-0002-6552-0176
Ai-Mei LiDepartment of Nephrology, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
Ya-Chun HanInstitute of Kidney Disease, Central South University, Changsha, Hunan Province, China.ORCID 0000-0002-8165-6698
Can-Hui PengDepartment of Clinical Laboratory, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.ORCID 0000-0002-4762-0333
Na SongDepartment of Nephrology, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
Ming YangInstitute of Kidney Disease, Central South University, Changsha, Hunan Province, China.ORCID 0000-0003-1698-0616
Ming ZhanInternational Medicine Department, Ningbo First Hospital, Zhejiang University, Ningbo, China.
Ling-Feng ZengInstitute of Kidney Disease, Central South University, Changsha, Hunan Province, China.ORCID 0000-0002-3194-3488
Pan-Ai SongInstitute of Kidney Disease, Central South University, Changsha, Hunan Province, China.
Wei ZhangDepartment of Nephrology, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
Shi-Qi TangDepartment of Nephrology, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
Hao ZhangDepartment of Nephrology, the Third Xiangya Hospital, Central South University, Changsha, Hunan Province, China.ORCID 0000-0002-2049-3485
Central South University · CNNingbo First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRenal tubular injury is an early characteristic of diabetic nephropathy (DN) that is related to mitochondrial dysfunction. In this study, we explore the effects and mechanisms of mitochondria-targeted peptide SS31 on renal tubulointerstitial injury in DN.

method40 C57BL/6 mice were randomly divided into control group, STZ group, STZ+SS31 group, and STZ+normal saline group. SS31 was intraperitoneally injected to the mice every other day for 24 weeks. Renal lesions and the expression of Drp1, Mfn1, Bcl-2, Bax, Caspase1, IL-1

resultsCompared with diabetic mice, the levels of serum creatinine and microalbuminuria were significantly decreased in the SS31 group. Renal tubulointerstitial fibrosis, oxidative stress, and apoptosis were observed in diabetic mice, while the pathological changes were reduced in the SS31-treatment group. SS31 could decrease the expression of Drp1, Bax, Caspase1, IL-1

conclusionSS31 protected renal tubulointerstitial injury in diabetic mice through a decrease in mitochondrial fragmentation via suppressing the expression of Drp1 and increasing the expression of Mfn1.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesHumansKidney TubulesMaleMiceMice, Inbred C57BLMitochondriaMitochondrial DynamicsNephritis, InterstitialOligopeptidesRandom AllocationReactive Oxygen Speciesarginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideOligopeptidesReactive Oxygen Species

Identifiers

PMID31281569
PMCPMC6589270
OpenAlexW2947183692

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.