ArticlePhysiological reports2014
Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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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.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- No influence of ischemic preconditioning on running economy.European journal of applied physiology · 2017Trial
- The contribution of cardiomyocyte hypercontracture to the burden of acute myocardial infarction: an update.Basic research in cardiology · 2025Review
- Slowly activating voltage-gated potassium current potentiation by ML277 is a novel cardioprotective intervention.PNAS nexus · 2023Article
- Citric Acid Cycle Metabolites Predict Infarct Size inInternational journal of molecular sciences · 2021Article
- Article
- Review
- Involvement of neuronal pathways in the protective effects of hindlimb perconditioning during renal ischemia.Experimental and therapeutic medicine · 2017Article
- The application of remote ischemic conditioning in cardiac surgery.F1000Research · 2017Review
- Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery.Basic research in cardiology · 2016Review
- Remote ischaemic conditioning and remodelling following myocardial infarction: current evidence and future perspectives.Heart failure reviews · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ischemic preconditioning (IPC) inhibits Ca(2+)-loading during ischemia which contributes to cardioprotection by inhibiting mechanical injury due to hypercontracture and biochemical injury through mitochondrial permeability transition (MPT) pores during reperfusion. However, whether remote-IPC reduced Ca(2+)-loading during ischemia and its subsequent involvement in inhibiting MPT pore formation during reperfusion has not been directly shown. We have developed a cellular model of remote IPC to look at the impact of remote conditioning on Ca(2+)-regulation and MPT pore opening during simulated ischemia and reperfusion, using fluorescence microscopy. Ventricular cardiomyocytes were isolated from control rat hearts, hearts preconditioned with three cycles of ischemia/reperfusion or naïve myocytes remotely conditioned with effluent collected from preconditioned hearts. Both conventional-IPC and remote-IPC reduced the loss of Ca(2+)-homeostasis and contractile function following reenergization of metabolically inhibited cells and protected myocytes against ischemia/reperfusion injury. However, only conventional-IPC reduced the Ca(2+)-loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na(+)-loading, reflecting a decrease in Na/H exchanger activity. Remote-IPC delayed opening of the MPT pores in response to ROS, which was dependent on PKCε and NOS-signaling. These data show that remote-IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca(2+)-loading in remote IPC. We suggest that inhibition of the MPT pore and not Ca(2+)-loading is the common link in cardioprotection between conventional and remote IPC.
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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.