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Antioxidants
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NADPH Oxidases in Health and Aging—2nd Edition
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NADPH Oxidases in Health and Aging—2nd Edition

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 September 2025 | Viewed by 3239

Special Issue Editors

Prof. Dr. Marschall S. Runge

E-Mail Website
Guest Editor
Frankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
Interests: oxidative stress; genetic/epigenetic modulators of CV function
Special Issues, Collections and Topics in MDPI journals
Dr. Nageswara R. Madamanchi

E-Mail Website
Guest Editor
Frankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
Interests: redox signaling; NADPH oxidases; VSMC biology;aging; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In view of the great response that we received for the previous Special Issue "NADPH Oxidases in Health and Aging", we decided to come up with its second edition.

Reactive oxygen species (ROS) play an important role in normal physiological processes such as blood pressure control and renal and central nervous system functions. However, ROS levels increase with aging, making it a risk factor for cardiovascular, pulmonary, renal, and neurological diseases. Nox family NADPH oxidases, whose sole function is the production of ROS, are differentially expressed in the cells of the above systems. NADPH oxidases are induced or activated by various risk factors associated with cardiovascular, pulmonary, renal, and neurological diseases, and the resulting persistent increase in ROS levels induce inflammation and fibrosis and the remodeling of the organ systems, increasing the disease severity. The concurrence of risk factors with old age adds to the disease burden. Even in apparently healthy people, differences in the expression pattern of NADPH oxidases in different tissues and organs affects disease risk based on ROS threshold levels, which has not been systematically addressed.

The aim for this Special Issue is to publish review articles on the regulation of redox signaling by NADPH oxidase in the physiology and pathophysiology of cardiovascular and pulmonary systems and neuronal networks, with emphasis on aging where pertinent.

We trust that the Special Issue will provide new insights into the function of NADPH oxidases in aging-associated increase in cardiovascular, pulmonary, renal, and neurological diseases.

Prof. Dr. Marschall S. Runge
Dr. Nageswara R. Madamanchi
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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • redox signaling
  • NADPH oxidases
  • reactive oxygen species (ROS)
  • aging

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Published Papers (1 paper)

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47 pages, 3709 KiB  
Review
Oxidative Stress in Kidney Injury and Hypertension
by Willaim J. Arendshorst, Aleksandr E. Vendrov, Nitin Kumar, Santhi K. Ganesh and Nageswara R. Madamanchi
Antioxidants 2024, 13(12), 1454; https://doi.org/10.3390/antiox13121454 - 27 Nov 2024
Cited by 1 | Viewed by 2847
Abstract
Hypertension (HTN) is a major contributor to kidney damage, leading to conditions such as nephrosclerosis and hypertensive nephropathy, significant causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD). HTN is also a risk factor for stroke and coronary heart disease. Oxidative [...] Read more.
Hypertension (HTN) is a major contributor to kidney damage, leading to conditions such as nephrosclerosis and hypertensive nephropathy, significant causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD). HTN is also a risk factor for stroke and coronary heart disease. Oxidative stress, inflammation, and activation of the renin–angiotensin–aldosterone system (RAAS) play critical roles in causing kidney injury in HTN. Genetic and environmental factors influence the susceptibility to hypertensive renal damage, with African American populations having a higher tendency due to genetic variants. Managing blood pressure (BP) effectively with treatments targeting RAAS activation, oxidative stress, and inflammation is crucial in preventing renal damage and the progression of HTN-related CKD and ESRD. Interactions between genetic and environmental factors impacting kidney function abnormalities are central to HTN development. Animal studies indicate that genetic factors significantly influence BP regulation. Anti-natriuretic mechanisms can reset the pressure–natriuresis relationship, requiring a higher BP to excrete sodium matched to intake. Activation of intrarenal angiotensin II receptors contributes to sodium retention and high BP. In HTN, the gut microbiome can affect BP by influencing energy metabolism and inflammatory pathways. Animal models, such as the spontaneously hypertensive rat and the chronic angiotensin II infusion model, mirror human essential hypertension and highlight the significance of the kidney in HTN pathogenesis. Overproduction of reactive oxygen species (ROS) plays a crucial role in the development and progression of HTN, impacting renal function and BP regulation. Targeting specific NADPH oxidase (NOX) isoforms to inhibit ROS production and enhance antioxidant mechanisms may improve renal structure and function while lowering blood pressure. Therapies like SGLT2 inhibitors and mineralocorticoid receptor antagonists have shown promise in reducing oxidative stress, inflammation, and RAAS activity, offering renal and antihypertensive protection in managing HTN and CKD. This review emphasizes the critical role of NOX in the development and progression of HTN, focusing on its impact on renal function and BP regulation. Effective BP management and targeting oxidative stress, inflammation, and RAAS activation, is crucial in preventing renal damage and the progression of HTN-related CKD and ESRD. Full article
(This article belongs to the Special Issue NADPH Oxidases in Health and Aging—2nd Edition)
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