Molecular pathways in cardiovascular disease under hypoxia:Mechanisms,biomarkers,and therapeutic targets
Izzatullo Abdullaev1
Ulugbek Gayibov1
Sirojiddin Omonturdiev1
Sobirova Fotima2
Sabina Gayibova1
Takhir Aripov1
1.A.S.Sadykov Institute of Bioorganic Chemistry,Science Academy of Uzbekistan,Laboratory of Plant CytoProtectors,Tashkent 100007,Uzbekistan2.Alfrganus University,Faculty of Medicine,Department of Pharmacy and Chemistry,Tashkent 100190,Uzbekistan
摘要：Chronic hypoxia is a key factor in the pathogenesis of cardiovascular diseases,including ischemia,heart failure,and hypertension.Under hypoxia,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.The mitochondrial ATP-sensitive potassium channel(mitoKATP)and mitochondrial permeability transition pore(mPTP)channels are particularly affected,contributing to membrane potential loss,cytochrome c release,and cell death.This review delves into 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 mitoKATP 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.
机标关键词：molecularpathwayshypoxiabiomarkerscardiovasculardiseasemechanismstargets
分类号：R54(心脏、血管（循环系）疾病)
论文发表日期：2025-05-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：16( 254-269 )
英文信息