ArticleRedox biology2017
Identification of transcriptome signature for myocardial reductive stress.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The transcriptional landscape of atrial fibrillation: A systematic review and meta-analysis.PloS one · 2025Pooled it
- The Calmodulin/Striatin Interaction Is Enhanced in Diabetic Hearts and Defines Novel Signaling Clusters Implicated in Cardiac Remodeling.ACS omega · 2026Article
- NRF2 deficit prevents pathologic Tau seeding and spreading in an induced tauopathy mouse model.Redox biology · 2026Article
- 401-Gene Signature of Myocardial Dysfunction in Human Heart Failure: A Transcriptomic Analysis.Cureus · 2025Article
- Differential gene expression and miRNA regulatory network in coronary slow flow.Scientific reports · 2024Article
- Influence of a Passive Tilt Test on the Proteomic Composition of the Blood of Healthy Humans.Bulletin of experimental biology and medicine · 2024Article
- Transgenic Expression of Nrf2 Induces a Pro-Reductive Stress and Adaptive Cardiac Remodeling in the Mouse.Genes · 2022Article
- Bioinformatic analysis of PD-1 checkpoint blockade response in influenza infection.BMC genomic data · 2022Article
- The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors.Antioxidants (Basel, Switzerland) · 2022Review
- Tandem Mass Tagging Based Identification of Proteome Signatures for Reductive Stress Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Induction of Premature Cell Senescence Stimulated by High Doses of Antioxidants Is Mediated by Endoplasmic Reticulum Stress.International journal of molecular sciences · 2021Article
- Identification of Nrf2-responsive microRNA networks as putative mediators of myocardial reductive stress.Scientific reports · 2021Article
- Implications of Oxidative and Nitrosative Post-Translational Modifications in Therapeutic Strategies against Reperfusion Damage.Antioxidants (Basel, Switzerland) · 2021Review
- Transcriptional Regulation of Structural and Functional Adaptations in a Developing Adulthood Myocardium.Cardiology and cardiovascular medicine · 2021Article
- Reductive stress in striated muscle cells.Cellular and molecular life sciences : CMLS · 2020Review
- Reductive Stress Causes Pathological Cardiac Remodeling and Diastolic Dysfunction.Antioxidants & redox signaling · 2020Article
- DNA damage-free iPS cells exhibit potential to yield competent cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy.Oxidative medicine and cellular longevity · 2020Review
- Exercise Mediated Nrf2 Signaling Protects the Myocardium From Isoproterenol-Induced Pathological Remodeling.Frontiers in cardiovascular medicine · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The nuclear factor erythroid 2 like 2 (Nfe2l2/Nrf2) is a master regulator of antioxidant gene transcription. We recently identified that constitutive activation of Nrf2 (CaNrf2) caused reductive stress (RS) in the myocardium. Here we investigate how chronic Nrf2 activation alters myocardial mRNA transcriptome in the hearts of CaNrf2 transgenic (TG-low and TG-high) mice using an unbiased integrated systems approach and next generation RNA sequencing followed by qRT-PCR methods. A total of 246 and 1031 differentially expressed genes (DEGs) were identified in the heart of TGL and TGH in relation to NTG littermates at ~ 6 months of age. Notably, the expression and validation of the transcripts were gene-dosage dependent and statistically significant. Ingenuity Pathway Analysis identified enriched biological processes and canonical pathways associated with myocardial RS in the CaNrf2-TG mice. In addition, an overrepresentation of xenobiotic metabolic signaling, glutathione-mediated detoxification, unfolded protein response, and protein ubiquitination was observed. Other, non-canonical signaling pathways identified include: eNOS, integrin-linked kinase, glucocorticoid receptor, PI3/AKT, actin cytoskeleton, cardiac hypertrophy, and the endoplasmic reticulum stress response. In conclusion, this mRNA profiling identified a "biosignature" for pro-reductive (TGL) and reductive stress (TGH) that can predict the onset, rate of progression, and clinical outcome of Nrf2-dependent myocardial complications. We anticipate that this global sequencing analysis will illuminate the undesirable effect of chronic Nrf2 signaling leading to RS-mediated pathogenesis besides providing important guidance for the application of Nrf2 activation-based cytoprotective strategies.
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