Mitochondrial reactive oxygen species generation in blood cells is associated with disease severity and exercise intolerance in heart failure patients
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Mitochondrial reactive oxygen species generation in blood cells is associated with disease severity and exercise intolerance in heart failure patients. / Shirakawa, Ryosuke; Yokota, Takashi; Nakajima, Takayuki; Takada, Shingo; Yamane, Miwako; Furihata, Takaaki; Maekawa, Satoshi; Nambu, Hideo; Katayama, Takashi; Fukushima, Arata; Saito, Akimichi; Ishimori, Naoki; Dela, Flemming; Kinugawa, Shintaro; Anzai, Toshihisa.
In: Scientific Reports, Vol. 9, 14709, 2019.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Mitochondrial reactive oxygen species generation in blood cells is associated with disease severity and exercise intolerance in heart failure patients
AU - Shirakawa, Ryosuke
AU - Yokota, Takashi
AU - Nakajima, Takayuki
AU - Takada, Shingo
AU - Yamane, Miwako
AU - Furihata, Takaaki
AU - Maekawa, Satoshi
AU - Nambu, Hideo
AU - Katayama, Takashi
AU - Fukushima, Arata
AU - Saito, Akimichi
AU - Ishimori, Naoki
AU - Dela, Flemming
AU - Kinugawa, Shintaro
AU - Anzai, Toshihisa
PY - 2019
Y1 - 2019
N2 - Systemic oxidative stress plays a key role in the development of chronic heart failure (CHF). We tested the hypothesis that mitochondrial reactive oxygen species (ROS) generation in circulating peripheral blood mononuclear cells (PBMCs) contributes to CHF progression. A total of 31 patients who had a history of hospital admission due to worsening HF were enrolled and grouped as having either mild CHF defined as NewYork Heart Association (NYHA) functional class I-II or moderate-to-severe CHF defined as NYHA functional class III. ROS levels in PBMC mitochondria were significantly increased in CHF patients with NYHA functional class III compared to those with NYHA functional class I-II, accompanied by impaired mitochondrial respiratory capacity in PBMCs. ROS generation in PBMC mitochondria was positively correlated with urinary 8-hydroxydeoxyguanosine, a systemic oxidative stress marker, in CHF patients. Importantly, mitochondrial ROS generation in PBMCs was directly correlated with plasma levels of B-type natriuretic peptide, a biomarker for severity of HF, and inversely correlated with peak oxygen uptake, a parameter of exercise capacity, in CHF patients. The study showed that ROS generation in PBMC mitochondria was higher in patients with advanced CHF, and it was associated with disease severity and exercise intolerance in CHF patients.
AB - Systemic oxidative stress plays a key role in the development of chronic heart failure (CHF). We tested the hypothesis that mitochondrial reactive oxygen species (ROS) generation in circulating peripheral blood mononuclear cells (PBMCs) contributes to CHF progression. A total of 31 patients who had a history of hospital admission due to worsening HF were enrolled and grouped as having either mild CHF defined as NewYork Heart Association (NYHA) functional class I-II or moderate-to-severe CHF defined as NYHA functional class III. ROS levels in PBMC mitochondria were significantly increased in CHF patients with NYHA functional class III compared to those with NYHA functional class I-II, accompanied by impaired mitochondrial respiratory capacity in PBMCs. ROS generation in PBMC mitochondria was positively correlated with urinary 8-hydroxydeoxyguanosine, a systemic oxidative stress marker, in CHF patients. Importantly, mitochondrial ROS generation in PBMCs was directly correlated with plasma levels of B-type natriuretic peptide, a biomarker for severity of HF, and inversely correlated with peak oxygen uptake, a parameter of exercise capacity, in CHF patients. The study showed that ROS generation in PBMC mitochondria was higher in patients with advanced CHF, and it was associated with disease severity and exercise intolerance in CHF patients.
U2 - 10.1038/s41598-019-51298-3
DO - 10.1038/s41598-019-51298-3
M3 - Journal article
C2 - 31605012
VL - 9
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 14709
ER -
ID: 229060005