ArticleFrontiers in physiology2013
Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS).
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 68 citations in OpenAlex.
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- Molecular Mechanisms of Oxidative Stress in Acute Kidney Injury: Targeting the Loci by Resveratrol.International journal of molecular sciences · 2023Review
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- miR-4432 Targets FGFBP1 in Human Endothelial Cells.Biology · 2023Article
- Tetrathiomolybdate Decreases the Expression of Alkaline Phosphatase in Dermal Papilla Cells by Increasing Mitochondrial ROS Production.International journal of molecular sciences · 2023Article
- Oxidative Stress in Assisted Reproductive Techniques, with a Focus on an Underestimated Risk Factor.Current issues in molecular biology · 2023Review
- Oxidative stress and mitochondrial dysfunction of granulosa cells in polycystic ovarian syndrome.Frontiers in medicine · 2023Review
- Role of mitochondrial reactive oxygen species in homeostasis regulation.Redox report : communications in free radical research · 2022Review
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- Effects of Zoniporide and BMA-1321 Compound on the Rate of Oxygen Absorption by Cardiomyocyte Mitochondria in Rats with Experimental Chronic Heart Failure.Bulletin of experimental biology and medicine · 2021Article
- Effect of phenylacetamide isolated fromPharmaceutical biology · 2020Article
- Mitochondria: A Galaxy in the Hematopoietic and Leukemic Stem Cell Universe.International journal of molecular sciences · 2020Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria represent major sources of basal reactive oxygen species (ROS) production of the cardiomyocyte. The role of ROS as signaling molecules that mediate different intracellular pathways has gained increasing interest among physiologists in the last years. In our lab, we have been studying the participation of mitochondrial ROS in the intracellular pathways triggered by the renin-angiotensin II-aldosterone system (RAAS) in the myocardium during the past few years. We have demonstrated that acute activation of cardiac RAAS induces mitochondrial ATP-dependent potassium channel (mitoKATP) opening with the consequent enhanced production of mitochondrial ROS. These oxidant molecules, in turn, activate membrane transporters, as sodium/hydrogen exchanger (NHE-1) and sodium/bicarbonate cotransporter (NBC) via the stimulation of the ROS-sensitive MAPK cascade. The stimulation of such effectors leads to an increase in cardiac contractility. In addition, it is feasible to suggest that a sustained enhanced production of mitochondrial ROS induced by chronic cardiac RAAS, and hence, chronic NHE-1 and NBC stimulation, would also result in the development of cardiac hypertrophy.
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