Evidence map›Paper›PMID 26078817›Full record

ArticleOxidative medicine and cellular longevity2015

Cardiac H2S Generation Is Reduced in Ageing Diabetic Mice.

Sheng Jin, Shi-Xin Pu, Cui-Lan Hou, Fen-Fen Ma, Na Li, Xing-Hui Li, Bo Tan, Bei-Bei Tao, Ming-Jie Wang, Yi-Chun Zhu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.8field-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

32 citing papers in PubMed, 71 citations in OpenAlex.

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  8. Endothelium as a Source and Target of HAntioxidants (Basel, Switzerland) · 2021
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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

10 authors at 3 institutions in 1 country.

Sheng JinShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China ; Department of Physiology, Hebei Medical University, Hebei 050017, China.
Shi-Xin PuShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Cui-Lan HouShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Fen-Fen MaDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China.
Na LiShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Xing-Hui LiShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Bo TanDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China.
Bei-Bei TaoShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Ming-Jie WangShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Yi-Chun ZhuShanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai 200032, China.
Shanghai Medical College of Fudan University · CNFudan University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims. To examine whether hydrogen sulfide (H2S) generation changed in ageing diabetic mouse hearts. Results. Compared to mice that were fed tap water only, mice that were fed 30% fructose solution for 15 months exhibited typical characteristics of a severe diabetic phenotype with cardiac hypertrophy, fibrosis, and dysfunction. H2S levels in plasma, heart tissues, and urine were significantly reduced in these mice as compared to those in controls. The expression of the H2S-generating enzymes, cystathionine γ-lyase and 3-mercaptopyruvate sulfurtransferase, was significantly decreased in the hearts of fructose-fed mice, whereas cystathionine-β-synthase levels were significantly increased. Conclusion. Our results suggest that this ageing diabetic mouse model developed diabetic cardiomyopathy and that H2S levels were reduced in the diabetic heart due to alterations in three H2S-producing enzymes, which may be involved in the pathogenesis of diabetic cardiomyopathy.

Indexed as

AgingAnimalsCells, CulturedCell SurvivalCystathionine beta-SynthaseCystathionine gamma-LyaseDiabetes Mellitus, ExperimentalDisease Models, AnimalGlucoseHeartHydrogen SulfideMaleMiceMice, Inbred C57BLMyocardiumMyocytes, Cardiac3-mercaptopyruvate sulphurtransferaseCystathionine beta-SynthaseCystathionine gamma-LyaseGlucoseHydrogen SulfideReactive Oxygen Speciessodium sulfideSulfidesSulfurtransferases

Identifiers

PMID26078817
PMCPMC4442299
OpenAlexW1515009635

What OpenQuestion holds

Textmetadata
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.