ReviewArchives of physiology and biochemistry2012
Mitochondrial mitophagic mechanisms of myocardial matrix metabolism and remodelling.
Review in Archives of physiology and biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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
16 citing papers in PubMed, 30 citations in OpenAlex.
- The complex link of the folate-homocysteine axis to myocardial hypertrophy and heart failure: from mechanistic exploration to clinical vision.Journal of advanced research · 2026Review
- Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Homocysteinylation of Fibrinogen: A Post-Translational Link to Thrombosis.International journal of molecular sciences · 2025Review
- Nicotinamide N-Methyltransferase (NNMT): A New Hope for Treating Aging and Age-Related Conditions.Metabolites · 2024Review
- Effect of hyperhomocysteinemia on rat cardiac sarcoplasmic reticulum.Molecular and cellular biochemistry · 2022Article
- Naringenin ameliorates homocysteine induced endothelial damage via the AMPKα/Sirt1 pathway.Journal of advanced research · 2021Article
- Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control.Theranostics · 2021Review
- Osthole down-regulates miR-30a and promotes autophagy to protect rats against myocardial ischemia/reperfusion injury.Turk gogus kalp damar cerrahisi dergisi · 2019Article
- Therapeutic targets for altering mitochondrial dysfunction associated with diabetic retinopathy.Expert opinion on therapeutic targets · 2018Review
- The effects of verapamil and its combinations with glutamate and glycine on cardiodynamics, coronary flow and oxidative stress in isolated rat heart.Journal of physiology and biochemistry · 2017Article
- The effects of the modulation of NMDA receptors by homocysteine thiolactone and dizocilpine on cardiodynamics and oxidative stress in isolated rat heart.Molecular and cellular biochemistry · 2015Article
- Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats.PloS one · 2015Article
- Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release.Physiological reviews · 2014Review
- Oxidative stress and autophagy in cardiovascular homeostasis.Antioxidants & redox signaling · 2014Review
- Pathogenesis of chronic cardiorenal syndrome: is there a role for oxidative stress?International journal of molecular sciences · 2013Review
- Mitochondria, myocardial remodeling, and cardiovascular disease.Current hypertension reports · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
High levels of homocysteine (Hcy), known as hyperhomocysteinmia (HHcy), are correlated with an increase in extracellular matrix remodelling (ECM) via the matrix metalloproteinases (MMPs) and plasminogen/plasmin system. This results in an increase deposition of collagen that leads to endothelial-myocyte (EM) and myocyte-myocyte (MM) uncoupling; the physiological consequences are a plethora of cardiovascular pathologies. Homocysteine-induced increase in intracellular and mitochondrial Ca(2+) plays an important role in increasing reactive oxygen species (ROS) within mitochondria and instigating mitophagy within the cell. This occurs via several Hcy-mitigated processes: agonizing N-methyl-d-aspartate receptor-1 (NMDA-R1), decreasing expression of peroxisome proliferator activator receptor (PPAR) [thereby increasing oxidation], impairing Ca(2+) handling via Na(+)/Ca(2+) exchanger (NCX1) and Sarco endoplasmic reticulum Ca(2+) ATPase (SERCA-2a). The end result is an increase in ROS that directly or indirectly lead to MMP activation within mitochondria or the cytoplasm. Hcy induces a mitochondrial permeability transition that allows MMPs to be released from mitochondria thereby metabolizing matrix and impairing cardiac function. Further work remains to be elucidated concerning the specific mitochondrial mitophagic mechanisms under which matrix metabolism and remodelling occurs. Moreover, the therapeutic implications of NMDA and PPAR ligands are some promise to patient.
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What Socratic 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 Socratic graph.