ReviewCardiovascular research2009
Regulation and pharmacology of the mitochondrial permeability transition pore.
Review in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 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
110 citing papers in PubMed, 232 citations in OpenAlex.
- A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury.Cell reports. Medicine · 2026Article
- Mitochondrial Impairment in Unloaded Postural Muscle: Mechanisms Driving Loss of Muscle Function and Mass.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- cGAS-STING-NF-κB Axis Mediates Rotenone-Induced NLRP3 Inflammasome Activation Through Mitochondrial DNA Release.Antioxidants (Basel, Switzerland) · 2025Article
- The hidden driver of osteoporosis: mitochondria-dominated inflammation.Cell communication and signaling : CCS · 2025Review
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Cladribine tablets in the new multiple sclerosis era.Therapeutic advances in neurological disorders · 2025Review
- Mitochondrial dysfunction: A promising therapeutic target for liver diseases.Genes & diseases · 2024Review
- The cytotoxic, genotoxic and mitotoxic effects ofAfrican health sciences · 2024Article
- Giant mitochondria in cardiomyocytes: cellular architecture in health and disease.Basic research in cardiology · 2023Review
- Review
- Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023Review
- Mitochondria: one of the vital hubs for molecular hydrogen's biological functions.Frontiers in cell and developmental biology · 2023Review
- Molecular signature associated with cladribine treatment in patients with multiple sclerosis.Frontiers in immunology · 2023Article
- A review of potential mechanisms and uses of SGLT2 inhibitors in ischemia-reperfusion phenomena.World journal of diabetes · 2022Review
- Plumbagin protects H9c2 cardiomyocytes against TBHP-induced cytotoxicity by alleviating ROS-induced apoptosis and modulating autophagy.Experimental and therapeutic medicine · 2022Article
- Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand-Addicted Pancreatic Cancer.Molecular cancer therapeutics · 2022Article
- Review
- Oxidative Stress Related to Plasmalemmal and Mitochondrial Phosphate Transporters in Vascular Calcification.Antioxidants (Basel, Switzerland) · 2022Review
- ATP Synthase KFunction (Oxford, England) · 2022Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The 'mitochondrial permeability transition', characterized by a sudden induced change of the inner mitochondrial membrane permeability for water as well as for small substances (</=1.5 kDa), has been known for three decades. Research interest in the entity responsible for this phenomenon, the 'mitochondrial permeability transition pore' (mPTP), has dramatically increased after demonstration that it plays a key role in the life and death decision in cells. Therefore, a better understanding of this phenomenon and its regulation by environmental stresses, kinase signalling, and pharmacological intervention is vital. The characterization of the molecular identity of the mPTP will allow identification of possible pharmacological targets and assist in drug design for its precise regulation. However, despite extensive research efforts, at this point the pore-forming core component(s) of the mPTP remain unidentified. Pivotal new genetic evidence has shown that components once believed to be core elements of the mPTP (namely mitochondrial adenine nucleotide translocator and cyclophilin D) are instead only mPTP regulators (or in the case of voltage-dependent anion channels, probably entirely dispensable). This review provides an update on the current state of knowledge regarding the regulation of the mPTP.
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.