Evidence map›Paper›PMID 36565415›Full record

ArticleMolecular biology reports2023

Mitochondrial transplantation protects against sepsis-induced myocardial dysfunction by modulating mitochondrial biogenesis and fission/fusion and inflammatory response.

Behnaz Mokhtari, Masoud Hamidi, Reza Badalzadeh, Ata Mahmoodpoor

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Effect of premorbid beta-blockers on cardiac function and clinical outcomes in septic patients: a retrospective study.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2026
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  15. MicroRNA-27b alleviates septic cardiomyopathy by targeting the Mff/MAVS axis.Frontiers in cellular and infection microbiology · 2025
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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

4 authors at 1 institution in 1 country.

Behnaz MokhtariMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID http://orcid.org/0000-0002-3355-9869
Masoud HamidiAnesthesiology Department, Ali Nasab Hospital, Tabriz, Iran.
Reza BadalzadehDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. badalzadehr@tbzmed.ac.ir.ORCID http://orcid.org/0000-0002-8092-7820
Ata MahmoodpoorEvidence-based Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. amahmoodpoor@yahoo.com.ORCID http://orcid.org/0000-0002-4361-6230
Tabriz University of Medical Sciences · IR

Funding

Drug Applied Research Center, Tabriz University of Medical Sciences IR.TBZMED.VCR.REC.1399.114
6 · The paper itself

Abstract

backgroundSepsis-induced myocardial dysfunction is associated with worse clinical outcomes and high mortality, but no effective therapeutic intervention has been explored, reinforcing the urgent need to develop innovative strategies. Mitochondrial dysfunction underlies the pathogenesis of sepsis-induced myocardial dysfunction. Herein, we assessed the effect of mitochondrial transplantation on sepsis-induced myocardial dysfunction in a rat model of cecal ligation and puncture (CLP)-induced sepsis.

methodsMale Wistar rats (n = 80, 12 weeks old, 250-300 g) were divided into groups with/without CLP-induced sepsis receiving mitochondrial transplantation in single or two repetitive injections (1 h or 1 and 7 h post-CLP, respectively). Mitochondria were isolated from donor rats and injected intravenously (400 µl of mitochondrial suspension containing 7.5 × 10

resultsMitotherapy significantly improved 72-hours survival (P < .05) and decreased LDH and cTn-I levels (P < .01). It also restored mitochondrial function and expression of mitochondrial biogenesis and fusion genes, and decreased the expression of mitochondrial fission gene and the levels of inflammatory cytokines (P < .05 to P < .01). Mitotherapy with repetitive injections at 1 and 7 h post-CLP provided noticeable mitoprotection in comparison with the group receiving mitotherapy at single injection.

conclusionMitotherapy improved mitochondrial function, biogenesis, and dynamic associated with SIRT-1/PGC-1α network and suppressed inflammatory response in CLP-induced sepsis model, therefore, offers a promising strategy to overcome life-threatening sepsis challenge.

Indexed as

CardiomyopathiesSepsisAnimalsCytokinesMaleMitochondriaOrganelle BiogenesisRatsRats, WistarCytokinesCardioprotectionMitochondrial transplantationMitoprotectionMyocardial dysfunctionSepsis

Identifiers

PMID36565415
OpenAlexW4312129488

What OpenQuestion holds

Textmetadata
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.