Camps Jordi, García-Heredia Anabel, Hernández-Aguilera Anna, Joven Jorge
Unitat de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut d'Investigació Sanitària Pere Virgili, C. Sant Joan s/n, Reus 43201, Catalonia, Spain.
Unitat de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut d'Investigació Sanitària Pere Virgili, C. Sant Joan s/n, Reus 43201, Catalonia, Spain.
Chem Biol Interact. 2016 Nov 25;259(Pt B):382-387. doi: 10.1016/j.cbi.2016.04.005. Epub 2016 Apr 7.
The most common non-communicable diseases (NCD) are obesity, cardiovascular disease, diabetes, cancer, chronic respiratory diseases, and neurological diseases. Together, they constitute the commonest cause of death and disability worldwide. Mitochondrial alterations, oxidative stress and inflammation underpin NCD and are molecular mechanisms playing major roles in the disease onset and natural history. Interrelations between the mechanisms of oxidative stress, inflammation and metabolism are, in the broadest sense of energy transformations, being increasingly recognized as part of the problem in NCD. Whether or not oxidative stress and inflammation are the causes or the consequences of cellular disturbances, they do significantly contribute to NCD. Paraoxonases are associated with mitochondria and mitochondria-associated membranes. They modulate mitochondria-dependent superoxide production, and prevent apoptosis. Their overexpression protects mitochondria from endoplasmic reticulum stress and subsequent mitochondrial dysfunction; highlighting that the anti-inflammatory effects of paraoxonases may be mediated, at least in part, by their protective role in mitochondria and associated organelle function. Since oxidative stress is implicated in the development of NCD (as a result of mitochondrial dysfunction), these data suggest that understanding the role and the molecular targets of paraoxonases may provide novel strategies of intervention in the treatment of these important diseases.
最常见的非传染性疾病包括肥胖症、心血管疾病、糖尿病、癌症、慢性呼吸道疾病和神经疾病。它们共同构成了全球范围内最常见的死亡和残疾原因。线粒体改变、氧化应激和炎症是导致非传染性疾病的基础，并且是在疾病发生和自然病程中起主要作用的分子机制。从能量转换的最广义角度来看，氧化应激、炎症和代谢机制之间的相互关系日益被视为非传染性疾病问题的一部分。无论氧化应激和炎症是细胞紊乱的原因还是后果，它们都对非传染性疾病有显著影响。对氧磷酶与线粒体及线粒体相关膜有关。它们调节线粒体依赖性超氧化物的产生，并防止细胞凋亡。它们的过表达可保护线粒体免受内质网应激及随后的线粒体功能障碍影响；这突出表明对氧磷酶的抗炎作用可能至少部分是通过其在线粒体及相关细胞器功能中的保护作用介导的。由于氧化应激与非传染性疾病的发展有关（由于线粒体功能障碍），这些数据表明，了解对氧磷酶的作用和分子靶点可能为治疗这些重要疾病提供新的干预策略。
