Mitochondria in Huntington’s disease:implications in pathogenesis and mitochondrial-targeted therapeutic strategies

作     者：Anamaria Jurcau Carolina Maria Jurcau Anamaria Jurcau;Carolina Maria Jurcau

作者机构：Department of Psycho-Neurosciences and RehabilitationFaculty of Medicine and PharmacyUniversity of OradeaOradeaRomania Neurology 3 WardClinical Emergency Hospital OradeaRomania Faculty of Medicine and PharmacyUniversity of OradeaRomania 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2023年第18卷第7期

页      面：1472-1477页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：antioxidants calcium homeostasis Huntington’s disease mitochondrial biogenesis mitochondrial fission/fusion mitochondrial trafficking oxidative phosphorylation oxidative stress SS peptides therapeutic intervention 

摘      要：Huntington’s disease is a genetic disease caused by expanded CAG repeats on exon 1 of the huntingtin gene located on chromosome *** evidence implicates impaired mitochondrial energetics,altered mitochondrial biogenesis and quality control,disturbed mitochondrial trafficking,oxidative stress and mitochondrial calcium dyshomeostasis in the pathogenesis of the ***,conventional mitochondrial-targeted molecules,such as cysteamine,creatine,coenzyme Q10,or triheptanoin,yielded negative or inconclusive ***,future therapeutic strategies,aiming to restore mitochondrial biogenesis,improving the fission/fusion balance,and improving mitochondrial trafficking,could prove useful tools in improving the phenotype of Huntington’s disease and,used in combination with genome-editing methods,could lead to a cure for the disease.