Molecular pathways in cardiovascular disease under hypoxia: Mechanisms, biomarkers, and therapeutic targets.

IF 2.2 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Izzatullo Ziyoyiddin O G Li Abdullaev, Ulugbek Gapparjanovich Gayibov, Sirojiddin Zoirovich Omonturdiev, Sobirova Fotima Azamjonovna, Sabina Narimanovna Gayibova, Takhir Fatikhovich Aripov
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Abstract

Chronic hypoxia is a key factor in the pathogenesis of cardiovascular diseases, including ischemia, heart failure, and hypertension. Under hypoxic conditions, oxygen deficiency disrupts oxidative phosphorylation in mitochondria, impairing ATP production and generating reactive oxygen species (ROS). These reactive species induce mitochondrial dysfunction, leading to oxidative stress, calcium imbalance, and activation of apoptosis pathways. Mitochondrial K-ATP (mitoK-ATP) and mitochondrial permeability transition pore (mPTP) channels are particularly affected, contributing to membrane potential loss, cytochrome C release, and cell death. This review explores the molecular mechanisms underlying hypoxia-induced cardiovascular diseases, with a focus on mitochondrial impairment, ion channel dysfunction, and ROS overproduction. Additionally, we examine hypoxia-inducible factor 1-alpha (HIF-1α) as a biomarker of cellular adaptation and discuss therapeutic strategies targeting mitochondrial function and oxidative stress. Antioxidants and compounds modulating key ion channels, such as K-ATP and mPTP, are highlighted as promising interventions for mitigating hypoxia-induced damage. Furthermore, we emphasize the potential of integrating in vitro, in vivo, and in silico studies to develop novel therapies aimed at preserving mitochondrial integrity and preventing cardiovascular diseases.

缺氧条件下心血管疾病的分子通路:机制、生物标志物和治疗靶点。
慢性缺氧是心血管疾病发病的关键因素,包括缺血、心力衰竭和高血压。在缺氧条件下,缺氧会破坏线粒体的氧化磷酸化,损害ATP的产生和活性氧(ROS)的产生。这些活性物质诱导线粒体功能障碍,导致氧化应激、钙失衡和细胞凋亡途径的激活。线粒体K-ATP (mitoK-ATP)和线粒体通透性过渡孔(mPTP)通道受到特别影响,导致膜电位损失、细胞色素C释放和细胞死亡。这篇综述探讨了缺氧诱导心血管疾病的分子机制,重点是线粒体损伤、离子通道功能障碍和ROS过量产生。此外,我们研究了缺氧诱导因子1- α (HIF-1α)作为细胞适应的生物标志物,并讨论了针对线粒体功能和氧化应激的治疗策略。抗氧化剂和调节关键离子通道的化合物,如K-ATP和mPTP,被强调为减轻缺氧引起的损伤的有希望的干预措施。此外,我们强调整合体外、体内和计算机研究的潜力,以开发旨在保持线粒体完整性和预防心血管疾病的新疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Biomedical Research
Journal of Biomedical Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
4.60
自引率
0.00%
发文量
69
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