Evidence map›Paper›PMID 40195349›Full record

ArticleScientific reports2025

Comparison of the proteomic landscape in experimental ischemia reperfusion with versus without ischemic preconditioning.

Yalda Kakaei, Shafaat Hussain, Ahmed Elmahdy, Evelin Berger, Aaron Shekka Espinosa, Valentyna Sevastianova, Zahra Sheybani, Amin Al-Awar, Mana Kalani, Sandeep Jha and 9 more

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

19 authors.

Yalda Kakaei *Department of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden. yalda.kakaei@gu.se.
Shafaat Hussain *Department of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Ahmed ElmahdyDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Evelin BergerProteomics Core Facility, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Aaron Shekka EspinosaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Valentyna SevastianovaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Zahra SheybaniDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Amin Al-AwarDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Mana KalaniDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Sandeep JhaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Ermir ZulfajDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Amirali NejatDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Abhishek JhaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Tetiana PylovaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Maryna KrasnikovaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Erik Axel AnderssonDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Vagner Ramon Rodrigues SilvaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Elmir OmerovicDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.
Björn RedforsDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, Bruna stråket 16, SU/S, 41345, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemic preconditioning (IPC) enhances myocardial resilience to ischemic injury. Myocardial stunning is a transient, reversible dysfunction, while necrosis involves irreversible cell death. The relationship between IPC, stunning, and necrosis is not well understood, requiring further molecular investigation. This study aimed to investigate the proteomic changes associated with IPC, focusing on its relationship with myocardial stunning and necrosis. A novel 13.5-minute ischemia-reperfusion (I/R) rat model was specifically chosen to induce myocardial stunning, providing a unique approach to assess IPC effects in this context. Rats underwent either IPC with two 5-minute ischemia/reperfusion cycles followed by a 13.5-minute ischemic period or the procedure without IPC (no ischemic preconditioning, NIPC). Myocardial samples were collected at early (T1) and 4-hour post-reperfusion (T2) time points for proteomic analysis. Protein levels were quantified by differential labeling using TMTpro reagents, and subsequent liquid chromatography-mass spectrometry. IPC induced upregulation of proteins involved in endocytosis and Fc gamma R-mediated phagocytosis pathways at T1, while downregulating proteins related to tissue remodeling, immune response, and coagulation at T2. Conversely, NIPC exhibited upregulation of proteins associated with tissue damage and inflammation. IPC rats demonstrated enhanced leukocyte migration, complement activation, and immune response between T1 and T2. Consistent proteomic changes were observed between T1 and T2 in IPC vs. NIPC groups, and common alterations between IPC T2 vs. T1 and NIPC T2 vs. T1 comparisons underline shared pathways in cardiac complement and coagulation cascades. Our study reveals distinct proteomic changes induced by IPC in the context of myocardial stunning and necrosis. IPC activates early protective pathways, attenuates tissue damage and inflammation, and preserves myocardial function. These findings underscore IPC's reparative potential and identify myocardial stunning as an important, transient adaptation, which may have implications for supportive clinical management in I/R.

Indexed as

Ischemic PreconditioningIschemic Preconditioning, MyocardialMyocardial Reperfusion InjuryProteomeProteomicsAnimalsDisease Models, AnimalMaleMyocardial StunningMyocardiumRatsRats, Sprague-DawleyProteomeCardiac proteomicsIschemia-reperfusion injuryMyocardial infarctionMyocardial ischemic preconditioningMyocardial stunningTherapeutic targets

Identifiers

PMID40195349
PMCPMC11976975

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.