Evidence map›Paper›PMID 35615579›Full record

ReviewOxidative medicine and cellular longevity2022

Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products.

Xin Su, Mingyang Zhou, Yingjian Li, Na An, Fan Yang, Guoxia Zhang, Lianjiang Xu, Hengwen Chen, Hongjin Wu, Yanwei Xing

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 20 citations in OpenAlex.

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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 4 institutions in 1 country.

Xin SuGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.ORCID https://orcid.org/0000-0002-5764-4355
Mingyang ZhouBeijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yingjian LiBeijing Anzhen Hospital, Capital Medical University, Beijing, China.
Na AnBeijing University of Chinese Medicine, Beijing, China.ORCID https://orcid.org/0000-0001-7794-2539
Fan YangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.ORCID https://orcid.org/0000-0002-8181-1627
Guoxia ZhangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.ORCID https://orcid.org/0000-0003-0646-8758
Lianjiang XuHebei Gangkou Hospital, Qinhuangdao, Hebei, China.
Hengwen ChenGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Hongjin WuBoao International Hospital, Shanghai University of Traditional Chinese Medicine, Qionghai, China.
Yanwei XingGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.ORCID https://orcid.org/0000-0002-1392-9738
Chinese Academy of Medical Sciences & Peking Union Medical College · CNCapital Medical University · CNBeijing University of Chinese Medicine · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic heart disease (IHD) is currently one of the leading causes of death among cardiovascular diseases worldwide. In addition, blood reflow and reperfusion paradoxically also lead to further death of cardiomyocytes and increase the infarct size. Multiple evidences indicated that mitochondrial function and structural disorders were the basic driving force of IHD. We summed up the latest evidence of the basic associations and underlying mechanisms of mitochondrial damage in the event of ischemia/reperfusion (I/R) injury. This review then reviewed natural plant products (NPPs) which have been demonstrated to mitochondria-targeted therapeutic effects during I/R injury and the potential pathways involved. We realized that NPPs mainly maintained the integrality of mitochondria membrane and ameliorated dysfunction, such as improving abnormal mitochondrial calcium handling and inhibiting oxidative stress, so as to protect cardiomyocytes during I/R injury. This information will improve our knowledge of mitochondrial biology and I/R-induced injury's pathogenesis and exhibit that NPPs hold promise for translation into potential therapies that target mitochondria.

Indexed as

Biological ProductsMyocardial IschemiaMyocardial Reperfusion InjuryHumansMitochondriaMitochondria, HeartMyocytes, CardiacOxidative StressBiological Products

Identifiers

PMID35615579
PMCPMC9126658
OpenAlexW4280522698

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.