Evidence map›Paper›PMID 36625783›Full record

ArticleACS nano2023

Intravenous Transplantation of an Ischemic-specific Peptide-TPP-mitochondrial Compound Alleviates Myocardial Ischemic Reperfusion Injury.

Xiaolei Sun, Hang Chen, Rifeng Gao, Yanan Qu, Ya Huang, Ning Zhang, Shiyu Hu, Fan Fan, Yunzeng Zou, Kai Hu and 3 more

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

Article in ACS nano, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
26.0field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 102 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

13 authors at 4 institutions in 1 country.

Xiaolei SunDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.ORCID 0000-0002-5260-379X
Hang ChenDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Rifeng GaoShanghai Fifth People's Hospital, Fudan University, Shanghai 200240, P.R. China.
Yanan QuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Ya HuangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Ning ZhangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.ORCID 0000-0001-6628-3953
Shiyu HuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Fan FanDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Yunzeng ZouDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Kai HuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Zhaoyang ChenDepartment of Cardiology, Fujian Medical Center for Cardiovascular Diseases, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China.
Junbo GeDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Aijun SunDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Sun Yat-sen University · CNFudan University · CNFujian Medical University · CNShanghai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is known that mitochondrial dysfunction is a critical factor involved in myocardial ischemia-reperfusion injury. Mitochondrial transplantation has been suggested as an effective therapeutic strategy to protect against myocardial ischemia-reperfusion injury. However, its clinical translation remains limited because it requires the local injection of mitochondria into the myocardium. Here, a polypeptide, CSTSMLKAC (PEP), bound to triphenylphosphonium cations (TPP+) effectively binds mitochondria to form a PEP-TPP-mitochondrial compound. Further investigation of this compound has revealed that the ischemia-sensing properties of PEP promote its translocation into the ischemic myocardium. Additionally, the targeting peptide, PEP, readily dissociates from the PEP-TPP-mitochondrial compound, allowing for the transplanted mitochondria to be efficiently internalized by cardiomyocytes or transferred to cardiomyocytes by endothelial cells. Mitochondrial transplantation promotes cardiomyocyte energetics and mechanical contraction, subsequently reducing cellular apoptosis, macrophage infiltration, and the pro-inflammatory response, all of which lead to attenuation of ischemia-reperfusion injury. Thus, this study provides promising evidence that the PEP-TPP-mitochondrial compound effectively promotes intravenous mitochondrial transplantation into the ischemic myocardium and subsequently ameliorates myocardial ischemia-reperfusion injury.

Indexed as

cardiomyocytesmitochondrial transplantationmyocardial ischemia−reperfusion injuryPEP−TPP−mitochondrial compoundtargeting peptide

Identifiers

PMID36625783
PMCPMC9878726
OpenAlexW4313986073

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.