ReviewInternational journal of molecular sciences2021
Mitochondria and Pharmacologic Cardiac Conditioning-At the Heart of Ischemic Injury.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Methyl rosmarinate alleviates myocardial ischemia-reperfusion injury in mice via triggering TGR5/AMPK signaling axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The effect of remote ischemic preconditioning on upper extremity strength in healthy male adults: an updated systematic review and meta-analysis.BMC sports science, medicine & rehabilitation · 2026Article
- Cardioprotective Signaling: Outline and Future Directions.Biomedicines · 2025Review
- Mitochondrial Transport Proteins in Cardiovascular Diseases: Metabolic Gatekeepers, Pathogenic Mediators and Therapeutic Targets.International journal of molecular sciences · 2025Review
- Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease.Biomedicines · 2025Review
- A Cell Autonomous Free fatty acid receptor 4 - ChemR23 Signaling Cascade Protects Cardiac Myocytes from Ischemic Injury.bioRxiv : the preprint server for biology · 2025Article
- Mitochondria-Targeted Biomaterials-Regulating Macrophage Polarization Opens New Perspectives for Disease Treatment.International journal of nanomedicine · 2025Review
- METTL3, m6A modification, and EGR1: interplay affecting myocardial I/R injury outcomes.Cell biology and toxicology · 2024Article
- Intra-operative anesthetic induced myocardial protection during cardiothoracic surgery: a literature review.Journal of thoracic disease · 2023Review
- cPKCγ-Modulated Autophagy Contributes to Ischemic Preconditioning-Induced Neuroprotection in Mice with Ischemic Stroke via mTOR-ULK1 Pathway.Translational stroke research · 2023Article
- Beneficial Effects of Halogenated Anesthetics in Cardiomyocytes: The Role of Mitochondria.Antioxidants (Basel, Switzerland) · 2023Review
- A Spectrofluorometric Method for Real-Time Graft Assessment and Patient Monitoring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning.International journal of molecular sciences · 2022Review
- Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress.International journal of molecular sciences · 2022Review
- Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products.Oxidative medicine and cellular longevity · 2022Review
- ATP Synthase KFunction (Oxford, England) · 2022Article
- Inhibition of PI3K/mTOR/KArchives of pharmacal research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.
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Registered trials
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.