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Antioxidants
Special Issues
Nrf2 and Cardiovascular Function, Diseases, and Therapeutic Targets
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Nrf2 and Cardiovascular Function, Diseases, and Therapeutic Targets

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 1943

Special Issue Editors

Dr. Gao Lie

E-Mail Website
Guest Editor
Department of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: heart failure; signaling pathway; oxidative stress; blood pressure regulation; hypertension; chronic heart failure; cardiac ischemia/reperfusion; cardiovascular system; skeletal muscle; Nrf2
Prof. Dr. Irving H. Zucker

E-Mail Website
Guest Editor
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: heart failure; hypertension; oxidative stress; antioxidant proteins; exercise; extracellular vesicle communication

Special Issue Information

Dear Colleagues,

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master transcription factor regulating a large group of genes and proteins involved in antioxidant and anti-inflammatory processes. Accumulating evidence suggests that Nrf2 plays a critical role in normal functioning of the heart, blood vessels, and autonomic nervous system by maintaining redox hemostasis. Conversely, impaired Nrf2 signaling contributes to the pathology of hypertension, heart failure, and atherosclerosis. Pharmacological activation of Nrf2 represents a promising therapeutic strategy. Both synthetic and natural compounds activating Nrf2, such as bardoxolone methyl, sulforaphane, curcumin, resveratrol, and others, have shown a reduction in oxidative stress and inflammation in the cardiovascular system and are currently being studied for their therapeutic potential in cardiovascular diseases.

This Special Issue aims to gather original research articles, reviews, perspectives, and short communications relevant to Nrf2 and the cardiovascular system. As Guest Editors, we invite you to contribute your research to this Special Issue for a comprehensive understanding the complex roles of Nrf2 in cardiovascular physiology and pathology with the hope of spurring interest in the development of effective Nrf2-targeted therapies.

Dr. Gao Lie
Prof. Dr. Irving H. Zucker
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • nuclear factor erythroid 2-related factor 2 (Nrf2)
  • Nrf2-targeted therapies
  • cardiovascular diseases
  • antioxidant
  • oxidative stress

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Published Papers (2 papers)

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18 pages, 5933 KB  
Article
Lifetime Deletion of Skeletal Muscle Keap1 Attenuates Aging-Induced Cardiac Dysfunction via an Nrf2–Antioxidant Mechanism
by Kanika Sharma, Sarah Pribil Pardun, Neha Dhyani, Irving H. Zucker, Bipin G. Nair, Sudarslal Sadasivan Nair, Vikas Kumar and Lie Gao
Antioxidants 2025, 14(12), 1491; https://doi.org/10.3390/antiox14121491 - 12 Dec 2025
Viewed by 561
Abstract
Background: Aging elevates reactive oxygen species (ROS) and weakens antioxidant defenses, contributing to cardiac dysfunction. The objective of this study was to determine whether sustained activation of skeletal muscle (SkM) Nrf2 preserves cardiac function during aging and to explore the underlying mechanisms, [...] Read more.
Background: Aging elevates reactive oxygen species (ROS) and weakens antioxidant defenses, contributing to cardiac dysfunction. The objective of this study was to determine whether sustained activation of skeletal muscle (SkM) Nrf2 preserves cardiac function during aging and to explore the underlying mechanisms, focusing on myocardial antioxidant pathways. Methods: Tamoxifen-induced SkM-specific Keap1 knockout male mice (iMS-Keap1flox/flox; SkM-Nrf2 overexpression) were divided into young wild-type (Y-WT), aged wild-type (A-WT), and aged knockout (A-KO) groups. Cardiac performance was evaluated by echocardiography and invasive hemodynamics. Myocardial proteomics identified differentially expressed proteins (DEPs) and enriched biological pathways. Results: Compared with Y-WT, A-WT mice showed impaired left ventricular function, including reduced ejection fraction, prolonged isovolumic relaxation time, blunted inotropic response to dobutamine, and elevated Tau index. These age-related deficits were partially reversed in A-KO mice. Proteomic analysis revealed 561 DEPs between A-WT and Y-WT, and 741 DEPs between A-KO and A-WT, enriched in calcium signaling, Nrf2-mediated oxidative stress response, oxidative phosphorylation, ROS detoxification, and cardiac-specific processes, such as hypertrophy, conduction, and dilated cardiomyopathy. Conclusions: Lifelong SkM-Nrf2 activation strengthens myocardial antioxidant capacity and alleviates age-related cardiac dysfunction. These data support an antioxidant crosstalk between skeletal muscle and the heart, highlighting a potential therapeutic target for aging-associated heart failure. Full article
(This article belongs to the Special Issue Nrf2 and Cardiovascular Function, Diseases, and Therapeutic Targets)
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13 pages, 7697 KB  
Article
Vitamin K3 Analog Phthiocol Protects Against High Phosphate-Induced Vascular Calcification in Chronic Kidney Disease
by Tsung-Jui Wu, Yi-Cheng Wang, Chia-Wen Lu, Chung-Jen Lee and Bang-Gee Hsu
Antioxidants 2025, 14(11), 1328; https://doi.org/10.3390/antiox14111328 - 4 Nov 2025
Viewed by 694
Abstract
Vascular calcification (VC) is a multifactorial pathological deposition of calcium in the vasculature and is associated with severe cardiovascular outcomes, particularly in patients with chronic kidney disease (CKD). Various vitamin K analogs have been found to influence the development of VC. We utilized [...] Read more.
Vascular calcification (VC) is a multifactorial pathological deposition of calcium in the vasculature and is associated with severe cardiovascular outcomes, particularly in patients with chronic kidney disease (CKD). Various vitamin K analogs have been found to influence the development of VC. We utilized a high-phosphate-induced VC model in mouse vascular smooth muscle cells (VSMCs) and developed an in vivo VC model using ApoE−/− mice subjected to 5/6 nephrectomy and fed an oral high-phosphorus diet to evaluate the effect of the vitamin K3 analog phthiocol. Transdermal glomerular filtration rate measurement, pulse wave velocity for aortic stiffness assessment, blood biochemical analysis, and pathological examinations were conducted. Phthiocol suppressed reactive oxygen species production and reduced subsequent cell death and calcification in a dose-dependent manner. It inhibited osteogenic trans-differentiation by restoring the PI3K/Akt pathway, activating Nrf2/HO-1 antioxidation signaling, and downregulating IL-1β and TNF-α. The high-phosphate diet in ApoE−/− CKD mice significantly induced dyslipidemia, renal impairment, hyperphosphatemia, aortic stiffness, and calcium deposition in aortic tissue compared to the control group. Phthiocol treatment markedly improved dyslipidemia, hyperphosphatemia, and aortic stiffness. The vitamin K3 analog phthiocol ameliorates phosphate-induced osteogenic trans-differentiation of VSMCs and subsequent VC by restoring the PI3K/Akt pathway and enhancing Nrf2/HO-1 antioxidant activity. Full article
(This article belongs to the Special Issue Nrf2 and Cardiovascular Function, Diseases, and Therapeutic Targets)
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