ReviewBiomedicines2025
Mitochondrial Permeability Transition Pore: The Cardiovascular Disease's Molecular Achilles Heel.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- TRPV1 Activation Is Associated with Improved Mitochondrial Function and Cardioprotection in Experimental Hypertension.Molecules (Basel, Switzerland) · 2026Article
- Mitochondrial Dysfunction at the Intersection of CKM Syndrome: Molecular Mechanisms and Path-to-Target Therapies.International journal of molecular sciences · 2026Review
- Article
- Molecular and Cellular Mechanisms of Cardioplegic Protection in Surgical Myocardial Revascularization.Cells · 2026Review
- Paraptosis, a new type of cell death that can be applied to cancer treatment.Frontiers in oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The mitochondrial permeability transition pore (mPTP) plays a central role in myocardial injury. Upon reperfusion after myocardial infarction, oxidative stress, calcium overload, and ATP depletion promote mPTP opening, leading to mitochondrial dysfunction, cell death, and infarct expansion. This process affects various cardiac cell types differently, contributing to complex pathological remodelling. Key mitochondrial events, such as disruption of bioenergetics parameters, impaired mitophagy, and oxidative stress, drive regulated cell death. Emerging therapies targeting mitochondrial biology, dynamics, and transplantation offer promising strategies to mitigate damage and improve cardiac outcomes. Considering the potential to improve cardiac outcomes and redefine therapeutic approaches in the management of cardiovascular disease, mPTP modulation represents a compelling therapeutic target in myocardial infarction and ischemia-reperfusion injury management.
Indexed as
Identifiers
What OpenQuestion holds
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.