ReviewBiochimica et biophysica acta2015
Reductive potential - a savior turns stressor in protein aggregation cardiomyopathy.
Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Advances regarding the mechanism of endoplasmic reticulum stress in diabetic kidney disease and pharmacological interventions (Review).Molecular medicine reports · 2026Review
- Global Proteomic Analysis Reveals Alterations in Differentially Expressed Proteins between Cardiopathic Lamin A/C Mutations.Journal of proteome research · 2024Article
- NRF2 activation induces NADH-reductive stress, providing a metabolic vulnerability in lung cancer.Cell metabolism · 2023Article
- Changing Perspectives from Oxidative Stress to Redox Signaling-Extracellular Redox Control in Translational Medicine.Antioxidants (Basel, Switzerland) · 2022Review
- Identification of Nrf2-responsive microRNA networks as putative mediators of myocardial reductive stress.Scientific reports · 2021Article
- Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection.International journal of molecular sciences · 2021Review
- Reductive stress promotes protein aggregation and impairs neurogenesis.Redox biology · 2020Article
- Reductive Stress Causes Pathological Cardiac Remodeling and Diastolic Dysfunction.Antioxidants & redox signaling · 2020Article
- Evaluation of an Antioxidant and Anti-inflammatory Cocktail Against Human Hypoactivity-Induced Skeletal Muscle Deconditioning.Frontiers in physiology · 2020Article
- Forced expression of miR-143 and -145 in cardiomyocytes induces cardiomyopathy with a reductive redox shift.Cellular & molecular biology letters · 2020Article
- Convergences of Life Sciences and Engineering in Understanding and Treating Heart Failure.Circulation research · 2019Article
- Selenium Nanoparticle Protection of Fibroblast Stress: Activation of ATF4 and Bcl-xL Expression.International journal of nanomedicine · 2019Article
- Glutathione "Redox Homeostasis" and Its Relation to Cardiovascular Disease.Oxidative medicine and cellular longevity · 2019Review
- Literature-Based Enrichment Insights into Redox Control of Vascular Biology.Oxidative medicine and cellular longevity · 2019Review
- Poor acute outcome in congestive heart failure is associated with increases in the plasma static oxidation-reduction potentials (sORP) in men but not in women.Redox report : communications in free radical research · 2017Article
- Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents.International journal of molecular sciences · 2017Review
- Constitutive activation of Nrf2 induces a stable reductive state in the mouse myocardium.Redox biology · 2017Article
- The Role of the Nrf2/ARE Antioxidant System in Preventing Cardiovascular Diseases.Diseases (Basel, Switzerland) · 2016Review
- Apocynin and Nox2 regulate NF-κB by modifying thioredoxin-1 redox-state.Scientific reports · 2016Article
- Role of Nrf2/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Redox homeostasis is essential for basal signaling of several physiological processes, but a unilateral shift towards an 'oxidative' or 'reductive' trait will alter intracellular redox milieu. Typically, such an event influences the structure and the native function of a cell or an organelle. Numerous experimental research and clinical trials over the last 6 decades have demonstrated that enhanced oxygen-derived free radicals constitute a major stimulus to trigger damage in several human diseases, including cardiovascular complications supporting the theory of oxidative stress (OS). However, until our key discovery, the dynamic interrelationship between "Reductive Stress (RS)" and cardiac health has been obscured by overwhelming OS studies (Rajasekaran et al., 2007). Notably, this seminal finding spurred considerable interest in investigations of other mechanistic insights, and thus far the results indicate a similar or stronger role for RS, as that of OS. In addition, from our own findings we strongly believe that constitutive activation of pathways that enable sustained generation of reducing equivalents of glutathione (GSH), reduced nicotinamide adenine dinucleotide phosphate (NADPH) will cause RS and impair the basal cellular signaling mechanisms operating through harmless pro-oxidative events, in turn, disrupting single and/or a combination of key cellular processes such as growth, maturation, differentiation, survival, death etc., that govern healthy cell physiology. Here, we have discussed the role of RS as a causal or contributing factor in relevant pathophysiology of a major cardiac disease of human origin.
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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.