Li 2015 Sci Rep
Li P, Wang B, Sun F, Li Y, Li Q, Lang H, Zhao Z, Gao P, Zhao Y, Shang Q, Liu D, Zhu Z (2015) Mitochondrial respiratory dysfunctions of blood mononuclear cells link with cardiac disturbance in patients with early-stage heart failure. Sci Rep 5:10229. |
Li Peng, Wang Bin, Sun Fang, Li Yingsha, Li Qiang, Lang Hongmei, Zhao Zhigang, Gao Peng, Zhao Yu, Shang Qianhui, Liu Daoyan, Zhu Zhiming (2015) Sci Rep
Abstract: 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+IIETS and CIIETS were 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 by in vitro experiments. 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. β’ Keywords: PBMC
β’ O2k-Network Lab: SG Singapore Hausenloy DJ, CN Chongqing Zhu Z
Labels: MiParea: Respiration, mt-Medicine, Patients
Pathology: Cardiovascular
Stress:Oxidative stress;RONS
Organism: Human
Tissue;cell: Blood cells, Lymphocyte
Preparation: Intact cells
Coupling state: LEAK, ROUTINE, OXPHOS, ET
Pathway: N, S, NS
HRR: Oxygraph-2k
CN, MitoEAGLE blood cells data