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Antioxidants
Special Issues
Oxidative Stress in Fertility and Infertility
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Oxidative Stress in Fertility and Infertility

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 2026 | Viewed by 2283

Special Issue Editor

Prof. Dr. Ying Cheong

E-Mail Website
Guest Editor
School of Human Development and Health, University of Southampton, Southampton SO17 1BJ, UK
Interests: oxidative stress; reproduction; fertility; gametogenesis; embryo development; implantation; pregnancy; miscarriage; antioxidants; redox biology; reproductive ageing; placental function; developmental programming; pre-eclampsia

Special Issue Information

Dear Colleagues,

Oxidative stress is a critical regulator of reproductive physiology, affecting gametogenesis, fertilisation, embryo development, implantation, and pregnancy outcomes. The disruption of redox balance has been linked to infertility, recurrent pregnancy loss, foetal growth restriction, and pre-eclampsia. This Special Issue will present cutting-edge basic, translational, and clinical research exploring oxidative stress in reproduction and development, novel antioxidant interventions, and implications for reproductive health. We welcome contributions from molecular biology, clinical medicine, and interdisciplinary fields.

Prof. Dr. Ying Cheong
Guest Editor

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

  • oxidative stress
  • reproduction
  • fertility
  • gametogenesis
  • embryo development
  • implantation
  • pregnancy
  • miscarriage
  • antioxidants
  • redox biology
  • reproductive ageing
  • placental function
  • developmental programming
  • pre-eclampsia

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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21 pages, 34393 KB  
Article
Oxidative Stress Mediated by Macrophages Promotes Angiogenesis and Early Development of Endometriosis
by Gene Chi Wai Man, Astrid Borchert, Tao Zhang, Sze Wan Hung, Hartmut Kühn and Chi Chiu Wang
Antioxidants 2026, 15(2), 159; https://doi.org/10.3390/antiox15020159 - 23 Jan 2026
Viewed by 1044
Abstract
Endometriosis is a hormone-dependent gynecological disease manifested by cyclic pelvic pain and female infertility. Although many studies have shown that neoangiogenesis plays an essential role in the development of early endometriosis, the underlying pathophysiological mechanisms remain unclear. Recent evidence suggests that macrophages play [...] Read more.
Endometriosis is a hormone-dependent gynecological disease manifested by cyclic pelvic pain and female infertility. Although many studies have shown that neoangiogenesis plays an essential role in the development of early endometriosis, the underlying pathophysiological mechanisms remain unclear. Recent evidence suggests that macrophages play an important role in the pathogenesis of endometriosis and that the hypoxia-inducible factor-1alpha (HIF-1α) may be involved, but when and how are largely unknown. Herein, we explore the role of macrophages in the early development of endometriosis using an in vivo subcutaneous implantation murine model. Upon depletion of macrophages, the subcutaneous injection of syngeneic endometrial material resulted in significant reduction in oxidative stress, endometriotic lesion size, and neovascularization. Likewise, inactivation of the lipid peroxidative gene Alox15 induced similar reduction in oxidative stress, lesion growth, and angiogenesis. Since HIF-1α is an important trigger of neoangiogenesis, we further administered a HIF-1α-specific inhibitor (PX-478) to our endometriotic model and further confirmed the same effects on the lesions. Taken together, these data suggest that an intact Alox15 pathway and HIF-1α signaling may play important roles in the macrophage-mediated oxidative stress and neovascularization of endometriosis in the early stages, suggesting anti-inflammation and antioxidation as potential therapeutic targets for the development of endometriosis. Full article
(This article belongs to the Special Issue Oxidative Stress in Fertility and Infertility)
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Review

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26 pages, 1455 KB  
Review
ROS–SUMO Crosstalk in Oxidative Stress: Disease Mechanisms and Reproductive Health
by Ann-Yae Na, Hyun-Shik Lee and Hong-Yeoul Ryu
Antioxidants 2026, 15(4), 453; https://doi.org/10.3390/antiox15040453 - 4 Apr 2026
Viewed by 836
Abstract
Oxidative stress disrupts protein function through direct oxidation and triggers adaptive post-translational modifications. Among these, small ubiquitin-like modifier (SUMO)-ylation mediates fast and reversible remodeling of nuclear and cytoplasmic proteins. Redox regulation of the SUMO E1–E2 conjugation complex and specific SUMO proteases, such as [...] Read more.
Oxidative stress disrupts protein function through direct oxidation and triggers adaptive post-translational modifications. Among these, small ubiquitin-like modifier (SUMO)-ylation mediates fast and reversible remodeling of nuclear and cytoplasmic proteins. Redox regulation of the SUMO E1–E2 conjugation complex and specific SUMO proteases, such as SENP1 and SENP3, allows ROS to influence SUMO turnover and substrate selectivity. This defines SUMOylation as a versatile stress-response module under oxidative stress. In this review, we describe oxidative stress-induced remodeling of SUMO conjugation and deconjugation, with a focus on SUMO2/3 responses that transiently adjust transcription, DNA damage repair, and nuclear body dynamics. We discuss disease-relevant SUMO targets and pathological alterations in SUMO regulation across four major disease categories: neurodegenerative diseases, cardiovascular disease, cancer, and diabetes/metabolic diseases. In addition, we summarize emerging evidence connecting redox-sensitive SUMO remodeling to germ-cell function and reproductive health. Together, these perspectives highlight the dual role of SUMOylation as both a driver of stress adaptation and a tractable target for informing therapeutic strategies targeting the SUMO pathway. Full article
(This article belongs to the Special Issue Oxidative Stress in Fertility and Infertility)
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