ReviewCurrent cardiology reviews2018
Reactive Oxygen Species as Intracellular Signaling Molecules in the Cardiovascular System.
Review in Current cardiology reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Pooled it
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- Neurovascular Uncoupling in Alzheimer's and Parkinson's Diseases: Mechanisms and Therapeutic Strategies.Brain sciences · 2026Review
- Nutritional Strategies and Aging: Current Evidence and Future Directions.Molecules (Basel, Switzerland) · 2026Review
- Article
- Interplay of oxidative stress and antioxidant mechanisms in cancer development and progression.Archives of toxicology · 2026Review
- From Defense to Disease: NADPH Oxidase in Cellular Function and Dysregulation.Journal of immunology research · 2026Review
- Panoramic description of ROS-based nanotechnology for osteomyelitis therapy: Challenges, opportunities, and prospects.Theranostics · 2026Review
- Reprogramming the Mitochondrion in Atherosclerosis: Targets for Vascular Protection.Antioxidants (Basel, Switzerland) · 2025Review
- Scavenging of reactive oxygen and nitrogen species using nanoparticles and their applications in disease management.RSC advances · 2025Review
- Metals in the human liver: An underappreciated risk factor of hepatic insulin resistance and associated pathophysiology.Environmental pollution (Barking, Essex : 1987) · 2025Review
- Brain nitric oxide and inflammation in chronic intermittent hypoxia: Contributors to cognitive impairment and hypertension.Brain, behavior, & immunity - health · 2025Review
- Mitochondrial ROS drive foam cell formation via STAT5 signaling in atherosclerosis.Science advances · 2025Article
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- Higher Food and Lifestyle Oxidative Balance Scores Decreases the Risk of Hypertension in Chinese Adults: A Population-Based Cross-Sectional Study.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Erectile Dysfunction and Oxidative Stress: A Narrative Review.International journal of molecular sciences · 2025Review
- Therapeutic potential of AAV2-shmTOR gene therapy in reducing retinal inflammation and preserving endothelial Integrity in age-related macular degeneration.Scientific reports · 2025Article
- The Role of Reductive Stress in the Pathogenesis of Endocrine-Related Metabolic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Molecular Insights in the Anticancer Activity of Natural Tocotrienols: Targeting Mitochondrial Metabolism and Cellular Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2025Review
- Plant-based bioactives and oxidative stress in reproduction: anti-inflammatory and metabolic protection mechanisms.Frontiers in nutrition · 2025Review
15 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
9 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRedox signaling plays an important role in the lives of cells. This signaling not only becomes apparent in pathologies but is also thought to be involved in maintaining physiological homeostasis. Reactive Oxygen Species (ROS) can activate protein kinases: CaMKII, PKG, PKA, ERK, PI3K, Akt, PKC, PDK, JNK, p38. It is unclear whether it is a direct interaction of ROS with these kinases or whether their activation is a consequence of inhibition of phosphatases. ROS have a biphasic effect on the transport of Ca2+ in the cell: on one hand, they activate the sarcoplasmic reticulum Ca2+-ATPase, which can reduce the level of Ca2+ in the cell, and on the other hand, they can inactivate Ca2+-ATPase of the plasma membrane and open the cation channels TRPM2, which promote Ca2+-loading and subsequent apoptosis. ROS inhibit the enzyme PHD2, which leads to the stabilization of HIF-α and the formation of the active transcription factor HIF.
conclusionActivation of STAT3 and STAT5, induced by cytokines or growth factors, may include activation of NADPH oxidase and enhancement of ROS production. Normal physiological production of ROS under the action of cytokines activates the JAK/STAT while excessive ROS production leads to their inhibition. ROS cause the activation of the transcription factor NF-κB. Physiological levels of ROS control cell proliferation and angiogenesis. ROS signaling is also involved in beneficial adaptations to survive ischemia and hypoxia, while further increases in ROS can trigger programmed cell death by the mechanism of apoptosis or autophagy. ROS formation in the myocardium can be reduced by moderate exercise.
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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.