Special Issue "Oxidative Stress and Antioxidants in Hypoxia and Human Pathophysiology Settings: Novel Pharmacological 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: 10 March 2024 | Viewed by 1417

Special Issue Editor

1. Departamento de Medicina Interna Oriente, Facultad de Medicina, Universidad de Chile, Santiago 7500922, Chile
2. Unidad de Paciente Crítico, Hospital del Salvador, Santiago 7500922, Chile
Interests: cardiovascular physiology and pathophysiology; animal models of intermittent hypoxia; cardiotoxicity; internal medicine; clinical trial

Special Issue Information

Dear Colleagues,

Hypoxic (HI) injury is defined as the worsening of organ/cellular dysfunction and cell death following reduction in blood flow due to organ targeting or increases in oxygen consumption in a related tissue. Restoration of blood flow is essential to salvage ischemic tissues. However, reperfusion itself causes further damage, contributing to reversible and irreversible changes in tissue viability and organ function, the basic pathophysiology of ischemia-reperfusion (IR) injury, especially oxidative stress, and cell death mechanism. When the blood supply is re-established, local inflammation and oxidative stress production increase, leading to secondary injury. Cell damage induced by prolonged ischemia must be distinguished from IR injury. It occurs in a wide range of organ systems, including the heart, lung, kidney, and brain. It may involve not only the ischemic organ itself but may also induce systemic damage to distant organs, potentially leading to multisystem organ failure, as different animal models have shown. Similar responses are seen in a human context, in patients exposed to acute and chronic hypoxia, from populations living in environments with low oxygen pressure, such as mountains (or high altitudes), to those suffering from conditions that induce hypoxia, such as what occurs at the cerebral and myocardial level with ischemic pathologies. Moreover, in some cancers, such as breast and colon, modulation of oxidative stress and tissue hypoxia could have a distant effect, for example, in the induction of cardiotoxicity.

This Special Issue is focused on the following topics:

-Current concepts of pathophysiology and therapies in cardiac HI and pharmacological preconditioning;

-Mechanisms of liver preconditioning in animal and clinical models of HI and IR injury;

-Current concepts of pathophysiology and therapies in cerebral HI and IR injury;

-Current concepts of anthracycline-induced cardiotoxicity in breast cancer: role of tumor microenvironment;

-Ex vivo models to reduce HI injury in organs for transplantation: role of antioxidants;

-Role of hypoxia in cardiovascular programing: mechanisms and potential therapeutic target with antioxidants;

-Role of microRNAs in the regulation of cardiac HI injury: animals and clinical settings.

Dr. Rodrigo L. Castillo
Guest Editor

Manuscript Submission Information

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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.


  • tissue hypoxia
  • reperfusion injury
  • hypoxic preconditioning
  • oxidative stress
  • antioxidants
  • hypoxic programing
  • microRNA
  • clinical hypoxic settings

Published Papers (1 paper)

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Nitroxide—HMP—Protects Human Trophoblast HTR-8/SVneo Cells from H2O2-Induced Oxidative Stress by Reducing the HIF1A Signaling Pathway
Antioxidants 2023, 12(8), 1578; https://doi.org/10.3390/antiox12081578 - 08 Aug 2023
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Preeclampsia (PE) is a pregnancy-specific syndrome affecting 5–7% of patients. There is no effective treatment available. Early abnormal placental development is associated with oxidative stress (OS) and a release of reactive oxygen species (ROS) in the placenta. This phenomenon leads to downstream signaling, [...] Read more.
Preeclampsia (PE) is a pregnancy-specific syndrome affecting 5–7% of patients. There is no effective treatment available. Early abnormal placental development is associated with oxidative stress (OS) and a release of reactive oxygen species (ROS) in the placenta. This phenomenon leads to downstream signaling, Hypoxia Inducible Factor 1A (HIF1A) stabilization and transcription of the anti-angiogenic factors soluble fms-like tyrosine kinase 1 (sFLT1) and soluble endoglin (sEng), which are known to cause endothelial and trophoblast dysfunction and cardinal features of PE: hypertension, proteinuria and, in severe cases, eclampsia. We tested whether 3-(Hydroxymethyl)-1-oxy-2,2,5,5-tetramethylpyrrolidine (HMP)—a nitroxide-type antioxidant molecule—can reduce placental OS and mitigate PE symptoms in vitro. We induced OS in human trophoblast (HTR-8/SVneo) cells with hydrogen peroxide (H2O2) and assessed whether modulating cell redox function with HMP reduces cell injury, mitochondrial stress and HIF1A and sFLT1 production. Pre-treatment with HMP reduced mitochondrial-derived ROS production, restored LC3B expression and reduced HIF1A and sFLT1 expression in H2O2-exposed HTR-8/SVneo trophoblast cells. HMP improved the mitochondrial electron chain enzyme activity, indicating that a reduction in OS alleviates mitochondrial stress and also reduces anti-angiogenic responses. In reducing placental trophoblast OS, HMP presents a potential novel therapeutic approach for the treatment of PE. Future investigation is warranted regarding the in vivo use of HMP. Full article
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