ReviewScientifica2013
Intracellular regulation of matrix metalloproteinase-2 activity: new strategies in treatment and protection of heart subjected to oxidative stress.
Review in Scientifica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 34 citations in OpenAlex.
- A review on MMP-2 modulating agents from natural and synthetic sources and their role in inflammatory bowel disease.Inflammopharmacology · 2026Review
- Context-dependent roles for ubiquitous mitochondrial creatine kinase CKMT1 in breast cancer progression.Cell reports · 2024Article
- Serum matrix metalloproteinase-2 as a predictor of level of hypoxemia and severity of obstructive sleep apnea.Sleep & breathing = Schlaf & Atmung · 2021Article
- Unravelling the Network of Nuclear Matrix Metalloproteinases for Targeted Drug Design.Biology · 2020Review
- Article
- Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases.Frontiers in physiology · 2020Review
- Paralogues of Mmp11 and Timp4 Interact during the Development of the Myotendinous Junction in the Zebrafish Embryo.Journal of developmental biology · 2019Article
- Intracellular Localization in Zebrafish Muscle and Conserved Sequence Features Suggest Roles for Gelatinase A Moonlighting in Sarcomere Maintenance.Biomedicines · 2019Article
- MicroRNA Networks Modulate Oxidative Stress in Cancer.International journal of molecular sciences · 2019Review
- Pharmacological Protection of Kidney Grafts from Cold Perfusion-Induced Injury.BioMed research international · 2019Review
- Human Adipose-Derived Hydrogel Characterization Based onStem cells international · 2019Article
- Role of Exercise-Induced Cardiac Remodeling in Ovariectomized Female Rats.Oxidative medicine and cellular longevity · 2018Article
- Matrix Metalloproteinases in Non-Neoplastic Disorders.International journal of molecular sciences · 2016Review
- The Role of Mitochondria and Oxidative/Antioxidative Imbalance in Pathobiology of Chronic Obstructive Pulmonary Disease.Oxidative medicine and cellular longevity · 2016Review
- Intracellular Cleavage of the Cx43 C-Terminal Domain by Matrix-Metalloproteases: A Novel Contributor to Inflammation?Mediators of inflammation · 2015Review
- Is there new hope for therapeutic matrix metalloproteinase inhibition?Nature reviews. Drug discovery · 2014Review
- Proinflammatory effects of diesel exhaust nanoparticles on scleroderma skin cells.Journal of immunology research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Much is known regarding cardiac energy metabolism in ischemia/reperfusion (I/R) injury. Under aerobic conditions, the heart prefers to metabolize fatty acids, which contribute to 60-80% of the required ATP. During ischemia, anaerobic glycolysis increases and becomes an important source of ATP for preservation of ion gradients. With reperfusion, fatty acid oxidation quickly recovers and again predominates as the major source of mitochondrial oxidative metabolism. Although a number of molecular mechanisms have been implicated in the development of I/R injury, their relative contributions remain to be determined. One such mechanism involves the proteolytic degradation of contractile proteins, such as troponin I (TnI), myosin heavy chain, titin, and the myosin light chains (MLC1 and MLC2) by matrix metalloproteinase-2 (MMP-2). However, very little is known about intracellular regulation of MMP-2 activity under physiological and pathological conditions. Greater understanding of the mechanisms that govern MMP-2 activity may lead to the development of new therapeutic strategies aimed at preservation of the contractile function of the heart subjected to myocardial infarction (MI) or I/R. This review discusses the intracellular mechanisms controlling MMP-2 activity and highlights a new intracellular therapeutic direction for the prevention and treatment of heart injury.
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.