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Molecular Biology of Hypoxia: 2nd Edition

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: 30 September 2026 | Viewed by 788

Special Issue Editor


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Guest Editor
Department of Sports and Para-Sports Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
Interests: biology; cartilage; synovium; ligament; meniscus; osteoarthritis; rheumatoid arthritis; HSP; HIF
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Special Issue Information

Dear Colleagues,

This Special Issue is the second volume of our Special Issue series, entitled “Molecular Biology of Hypoxia”.

Oxygen is essential for the survival of cells and organs in the body, and hypoxic conditions can disrupt a wide range of functional and metabolic systems. However, several types of cells and tissues have a reserve capacity that allows for the mobilization of defense mechanisms for survival in response to relatively acute and less severe hypoxic conditions. In vivo, tissues such as the cornea and articular cartilage lack blood flow and maintain homeostasis in a normoxic environment. The response to these hypoxic conditions results from molecular processes that occur at the cellular level. Central to this response are hypoxia-inducible factors (HIFs), which are downregulated in steady-state oxygen and upregulated in hypoxia, and have also attracted attention as therapeutic targets for various diseases. Intensive studies on the mechanisms that contribute to the development of hypoxia tolerance in cells and tissues are theoretically important as well as necessary to address numerous problems in practical medicine. Studies in this field have significantly advanced our understanding; however, several important questions remain unanswered. Therefore, this Special Issue focuses on the “Molecular Biology of Hypoxia” in various cells and tissues, including the heart, brain, kidneys, articular cartilage, and tumors, and we invite papers that report novel findings and answer questions that currently remain unanswered.

Dr. Yuji Arai
Guest Editor

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Keywords

  • hypoxia
  • HIFs
  • normoxic environment

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Published Papers (1 paper)

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Research

15 pages, 3468 KB  
Article
Effects of Gelatin Hydrolysate from Bigeye Snapper (Priacanthus tayenus) Skin in Mitigating Oxidative Stress in Chronic Cerebral Hypoperfusion Rats
by Jirakhamon Sengking, Phakkawat Thangwong, Pranglada Jearjaroen, Nuttapong Yawoot, Sutee Wangtueai, Jiraporn Tocharus and Chainarong Tocharus
Int. J. Mol. Sci. 2026, 27(6), 2856; https://doi.org/10.3390/ijms27062856 - 21 Mar 2026
Viewed by 431
Abstract
Gelatin hydrolysate (GH), a bioactive compound derived from collagen, has demonstrated potential therapeutic benefits in various medical conditions. However, its effects on chronic cerebral hypoperfusion-induced vascular dementia remain underexplored. This study aimed to investigate the anti-oxidative stress effects of GH in alleviating brain [...] Read more.
Gelatin hydrolysate (GH), a bioactive compound derived from collagen, has demonstrated potential therapeutic benefits in various medical conditions. However, its effects on chronic cerebral hypoperfusion-induced vascular dementia remain underexplored. This study aimed to investigate the anti-oxidative stress effects of GH in alleviating brain damage and cognitive impairment in CCH-induced rats. Male Wistar rats underwent bilateral common carotid artery occlusion to induce CCH and were randomly divided into five groups: (1) sham, (2) 2-vessel occlusion (2VO), (3) 2VO + 250 mg/kg GH, (4) 2VO + 500 mg/kg GH, and (5) 2VO + piracetam. Treatments were administered for 35 days of post-operation. GH treatment significantly mitigated oxidative stress, as evidenced by reduced levels of reactive oxygen species (ROS), nitric oxide (NO), and the expression of 4-hydroxynonenal (4-HNE) and NADPH oxidase 4 (NOX4). Furthermore, GH exhibited antioxidant activity by upregulating superoxide dismutase (SOD) levels via nuclear factor E2-related factor 2 (Nrf-2) activation. This, in turn, reduced neuronal apoptosis by decreasing Bax and cleaved-caspase 3 levels and increasing Bcl-2 expression. Additionally, GH treatment ameliorated Tau protein hyperphosphorylation and improved synaptic function. Overall, GH exerted neuroprotective effects against oxidative stress-related neuronal damage and enhanced neuroplasticity, learning, and memory in rats with CCH-induced cognitive impairment. Full article
(This article belongs to the Special Issue Molecular Biology of Hypoxia: 2nd Edition)
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