Mitochondrial respiratory dysfunctions of blood mononuclear cells link with cardiac disturbance in patients with early-stage heart failure.

Mitochondrial respiratory dysfunctions of blood mononuclear cells link with cardiac disturbance in patients with early-stage heart failure.
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血液单核细胞的线粒体呼吸功能障碍与早期心力衰竭患者的心脏功能障碍有关

DOI:
10.1038/srep10229
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发表时间:
2015-05-28
期刊:
影响因子:
4.6
通讯作者:
Zhu Z
Zhu Z
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Li P;Wang B;Sun F;Li Y;Li Q;Lang H;Zhao Z;Gao P;Zhao Y;Shang Q;Liu D;Zhu Z

文献摘要

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具有心脏代谢危险因素和无症状心脏肥大的患者是早期心力衰竭(HF)的标志。我们假设,外周血单个核细胞(PBMC)的线粒体呼吸功能障碍可能与炎症和氧化应激在早期HF患者并发心脏代谢危险因素。共入组49名受试者,其中25名患有心脏肥大和功能障碍的早期HF患者(A和B期)和24名健康对照。结果表明,在早期HF患者中,过度炎症和抗氧化能力降低与心脏异常密切相关。此外,早期HF患者的线粒体呼吸功能参数R、CIOXPHOS、CIIOXPHOS、CI+IIOXPHOS、CI+ IIETS和CIIETS均显著降低。有趣的是,这些呼吸参数与参与者的炎症和抗氧化能力相关。最后,心脏代谢危险因素,如作为盐摄入量和血压与线粒体呼吸功能障碍有关,这一点在体外实验中得到了进一步验证。我们的研究表明,心脏代谢危险因素介导的PBMCs线粒体呼吸功能障碍与早期HF的细胞炎症/氧化应激和心脏功能障碍有关。
Patients with cardiometabolic risk factors and asymptomatic cardiac hypertrophy are hallmarks of early-stage heart failure (HF). We hypothesized that mitochondrial respiratory dysfunctions of peripheral blood mononuclear cells (PBMCs) may be associated with inflammation and oxidative stress in early-stage HF patients complicated with cardiometabolic risk factors. Totally 49 subjects were enrolled with 25 early-stage HF patients (stages A and B) having cardiac hypertrophy and dysfunction and 24 healthy controls. It showed that excessive inflammation and reduced antioxidant capacity were closely associated with cardiac abnormalities in early-stage HF patients. Furthermore, the values of mitochondrial respiratory functional parameters R, CIOXPHOS, CIIOXPHOS, CI+IIOXPHOS,CI+IIETSand CIIETSwere significantly lowered in early-stage HF patients. Interestingly, these respiratory parameters were correlated with inflammation and antioxidant capacity in participants. Finally, cardiometabolic risk factors such as salt intake and blood pressure were related to the mitochondrial respiratory dysfunctions, which were further validated byin vitroexperiments. Our study indicated that cardiometabolic risk factor-mediated mitochondrial respiratory dysfunctions of PBMCs link with the cellular inflammation / oxidative stress and cardiac disturbance in early-stage HF.