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Hypoxia: Molecular Mechanism and Health Effects
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Hypoxia: Molecular Mechanism and Health Effects

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 July 2026 | Viewed by 5663

Special Issue Editor

Dr. Pinar Uysal-Onganer

E-Mail Website
Guest Editor
Cancer Research Group, School of Life Sciences, College of Liberal Arts & Sciences, University of Westminster, London, UK
Interests: non-coding RNAs; molecular oncology; tumour microenvironment; Wnt signalling; prostate cancer; breast cancer; pancreatic ductal adenocarcinoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hypoxia, a condition characterized by reduced oxygen availability, has a critical role in various physiological and pathological processes. It is a key factor in the progression of diseases such as cancer, cardiovascular disorders, neurodegenerative diseases, and chronic inflammatory conditions. At the cellular level, hypoxia triggers complex molecular mechanisms involving hypoxia-inducible factors (HIFs), oxidative stress, mitochondrial dysfunction, and metabolic reprogramming, which collectively influence cell survival, proliferation, and adaptation.

This Special Issue, "Hypoxia: Molecular Mechanism and Health Effects", aims to bring together cutting-edge research that explores the intricate molecular pathways activated by hypoxia and their implications for health and disease. We welcome submissions that investigate the cellular responses to hypoxia, the role of hypoxia in disease pathogenesis, and potential therapeutic strategies to mitigate hypoxia-induced damage. Studies focusing on the crosstalk between hypoxia and other signalling pathways, the role of hypoxia in tissue regeneration, and the development of novel hypoxia-targeted therapies are particularly encouraged.

The aim of this Special Issue is to evaluate the current advances in hypoxia research, offering insights into the molecular underpinnings of hypoxia-related diseases and paving the way for the development of innovative therapeutic approaches. We invite researchers from diverse fields, including molecular biology, biochemistry, and pharmacology, to contribute original research articles, reviews, and perspectives that enhance our understanding of hypoxia and its wide-ranging impacts on human health.

Dr. Pinar Uysal-Onganer
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • hypoxia
  • inflammation
  • oxidative stress
  • metabolic conditions
  • hypoxia-inducible factors (HIFs)
  • oxidative stress
  • mitochondrial dysfunction
  • angiogenesis
  • metabolic reprogramming
  • apoptosis

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Published Papers (4 papers)

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Research

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22 pages, 4170 KB  
Article
Short- and Long-Term Effects of Sodium Phenylbutyrate on White Matter and Sensorimotor and Cognitive Behavior in a Mild Murine Model of Encephalopathy of Prematurity
by Marie-Anne Le Ray, Cyann Larralde, Lou Legouez, Stéphane Marret, Jean-Baptiste Muller, Bruno J. Gonzalez and Carine Cleren
Int. J. Mol. Sci. 2025, 26(24), 12099; https://doi.org/10.3390/ijms262412099 - 16 Dec 2025
Viewed by 144
Abstract
Perinatal asphyxia (PA) remains a common cause of neonatal death and long-term disability, with an incidence of 20 per 1000 live births. Even mild PA, without significant neurological distress at birth, is linked to neurodevelopmental disorders. Premature babies are at high risk for [...] Read more.
Perinatal asphyxia (PA) remains a common cause of neonatal death and long-term disability, with an incidence of 20 per 1000 live births. Even mild PA, without significant neurological distress at birth, is linked to neurodevelopmental disorders. Premature babies are at high risk for both PA and long-term neurobehavioral deficits. The use of peripherally inserted central venous catheters in neonatal intensive care units has reduced mortality and morbidity in preterms. Given their prevalent use and associated complications, such as thrombosis, the present study aimed to investigate the effects of hypoxia associated with the ligation of the external jugular vein (JH model) in 5-day-old mice, whose central nervous system development shares similarities with that of human preterms. Diffuse white matter (WM) injury is associated with later neurodisabilities following very premature birth before 32 weeks of gestation. The present study aimed to investigate whether the murine JH model replicates a key phenotype of non-cystic WM injury, namely permanent hypomyelination and sensorimotor deficits. The second aim was to determine whether sodium phenylbutyrate (PBA), which is already prescribed in neonates for another indication, could prevent these disabilities. JH induced lasting dysmyelination in males, not prevented by PBA, contrary to the discrete JH-induced neurobehavioral deficits observed in both sexes in the short and long term. Full article
(This article belongs to the Special Issue Hypoxia: Molecular Mechanism and Health Effects)
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22 pages, 14854 KB  
Article
Multiomics Analysis Reveals Role of ncRNA in Hypoxia of Mouse Brain Microvascular Endothelial Cells
by Qixin Shi, Shuai Zhang, Shaohua Li, Bin Zhang, Jin Xu, Yun-Gang Bai, Man-Jiang Xie and Jin Ma
Int. J. Mol. Sci. 2025, 26(12), 5629; https://doi.org/10.3390/ijms26125629 - 12 Jun 2025
Viewed by 1153
Abstract
Hypoxia leads to endothelial dysfunction and increased blood–brain barrier (BBB) permeability, promoting the incidence of diseases such as stroke and acute high-altitude illness. Brain microvascular endothelial cells (BMECs) are important structural and functional components of the BBB; however, the molecular changes that occur [...] Read more.
Hypoxia leads to endothelial dysfunction and increased blood–brain barrier (BBB) permeability, promoting the incidence of diseases such as stroke and acute high-altitude illness. Brain microvascular endothelial cells (BMECs) are important structural and functional components of the BBB; however, the molecular changes that occur in BMECs during hypoxia remain unknown. We reported the molecular and functional changes in BMECs under hypoxia through whole-transcriptome sequencing, small RNA microarray, TMT quantitative proteomic, and untargeted metabolomic analyses. We found that hypoxia affected pathways such as ncRNA processing, the HIF-1 signaling pathway, the cell cycle, DNA replication, glucose metabolism, protein synthesis, and inflammation pathways. ncRNA processing was significantly downregulated. However, the levels of some miRNAs, tRNAs, tsRNAs, snoRNAs, lncRNAs, and circRNAs were significantly upregulated under hypoxia. These results suggest that ncRNAs may play an important role in oxidative stress and cellular adaptation to hypoxia, helping us understand the pathological process of BBB injury and providing potential targets for the treatment of BBB-related cerebrovascular diseases. Full article
(This article belongs to the Special Issue Hypoxia: Molecular Mechanism and Health Effects)
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Review

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24 pages, 1060 KB  
Review
Biological Regulation of HIF-1α and Its Role in Therapeutic Angiogenesis for Treatment of Ischemic Cardiovascular Disease
by Ethan Carmichael, Anne-Isabelle S. Reme, Patrick J. Bosco, Yulexi Y. Ortiz, Daniela Alexandra Ramos, Katherine Gomez, Bao-Ngoc Nguyen, Arash Bornak, Zhao-Jun Liu and Omaida C. Velazquez
Int. J. Mol. Sci. 2025, 26(22), 11236; https://doi.org/10.3390/ijms262211236 - 20 Nov 2025
Viewed by 1035
Abstract
Hypoxia, characterized by insufficient oxygen saturation, triggers a wide array of vascular responses aimed at enhancing cell survival and proliferation. This process is primarily driven by the activation of oxygen-sensing hypoxia-inducible factors (HIFs). HIF-1α, a key mediator in this context, plays a crucial [...] Read more.
Hypoxia, characterized by insufficient oxygen saturation, triggers a wide array of vascular responses aimed at enhancing cell survival and proliferation. This process is primarily driven by the activation of oxygen-sensing hypoxia-inducible factors (HIFs). HIF-1α, a key mediator in this context, plays a crucial role in vascular restructuring in response to low oxygen tension and oxygen-independent signaling pathways, making it a promising therapeutic target for ischemic cardiovascular diseases such as peripheral artery disease and coronary artery disease. In this review, we explore both oxygen-dependent and oxygen-independent mechanisms of HIF-1α regulation, the role of the HIF protein family in vessel collateralization, and translational efforts to leverage HIF-1α‘s pivotal role in hypoxia signaling for the development of clinical treatments for ischemic cardiovascular disease. Full article
(This article belongs to the Special Issue Hypoxia: Molecular Mechanism and Health Effects)
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18 pages, 929 KB  
Review
From Hypoxia to Bone: Reprogramming the Prostate Cancer Metastatic Cascade
by Melissa Santos, Sarah Koushyar, Dafydd Alwyn Dart and Pinar Uysal-Onganer
Int. J. Mol. Sci. 2025, 26(15), 7452; https://doi.org/10.3390/ijms26157452 - 1 Aug 2025
Cited by 1 | Viewed by 1621
Abstract
Bone is the most frequent site of distant metastasis in advanced prostate cancer (PCa), contributing substantially to patient morbidity and mortality. Hypoxia, a defining feature of the solid tumour microenvironment, plays a pivotal role in driving bone-tropic progression by promoting epithelial-to-mesenchymal transition (EMT), [...] Read more.
Bone is the most frequent site of distant metastasis in advanced prostate cancer (PCa), contributing substantially to patient morbidity and mortality. Hypoxia, a defining feature of the solid tumour microenvironment, plays a pivotal role in driving bone-tropic progression by promoting epithelial-to-mesenchymal transition (EMT), cancer stemness, extracellular matrix (ECM) remodelling, and activation of key signalling pathways such as Wingless/Integrated (Wnt) Wnt/β-catenin and PI3K/Akt. Hypoxia also enhances the secretion of extracellular vesicles (EVs), enriched with pro-metastatic cargos, and upregulates bone-homing molecules including CXCR4, integrins, and PIM kinases, fostering pre-metastatic niche formation and skeletal colonisation. In this review, we analysed current evidence on how hypoxia orchestrates PCa dissemination to bone, focusing on the molecular crosstalk between HIF signalling, Wnt activation, EV-mediated communication, and cellular plasticity. We further explore therapeutic strategies targeting hypoxia-related pathways, such as HIF inhibitors, hypoxia-activated prodrugs, and Wnt antagonists, with an emphasis on overcoming therapy resistance in castration-resistant PCa (CRPC). By examining the mechanistic underpinnings of hypoxia-driven bone metastasis, we highlight promising translational avenues for improving patient outcomes in advanced PCa. Full article
(This article belongs to the Special Issue Hypoxia: Molecular Mechanism and Health Effects)
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