Plasma Heme Oxygenase-1 Levels and Carotid Atherosclerosis

Kishimoto, Yoshimi; Sasaki, Kenji; Saita, Emi; Niki, Hanako; Ohmori, Reiko; Kondo, Kazuo; Momiyama, Yukihiko

doi:10.1161/strokeaha.118.022256

Cited by 17 publications

(14 citation statements)

References 13 publications

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“…Although the precise mechanisms of secretion and the significance of the extracellular HO-1 remain to be determined, HO-1 is known to be released into the plasma by leukocytes, macrophages, smooth muscle cells, and endothelial cells that are activated or damaged by oxidative stress or inflammation [4]. Kishimoto et al hypothesized that plasma HO-1 levels may be associated with the presence and severity of carotid atherosclerosis, and they measured the plasma HO-1 levels in 136 consecutive subjects (mean age 66 ± 9 years) who underwent carotid ultrasonography for a medical check-up to evaluate atherosclerosis [25]. The study was the first to reveal that the plasma HO-1 levels were significantly higher in the subjects with carotid plaque than in those without plaque (median 0.56 versus 0.44 ng/mL, p < 0.05), and the levels were stepwisely increased depending on the severity of plaque, defined as the plaque score (Figure 1).…”

Section: Ho-1 Expression In Patients With Atherosclerotic Diseasesmentioning

confidence: 99%

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The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases

Kishimoto

Kondo

Momiyama

2019

IJMS

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Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme to generate ferrous iron, carbon monoxide (CO), and biliverdin, which is subsequently converted to bilirubin. These products have anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-thrombotic properties. Although HO-1 is expressed at low levels in most tissues under basal conditions, it is highly inducible in response to various pathophysiological stresses/stimuli. HO-1 induction is thus thought to be an adaptive defense system that functions to protect cells and tissues against injury in many disease settings. In atherosclerosis, HO-1 may play a protective role against the progression of atherosclerosis, mainly due to the degradation of pro-oxidant heme, the generation of anti-oxidants biliverdin and bilirubin and the production of vasodilator CO. In animal models, a lack of HO-1 was shown to accelerate atherosclerosis, whereas HO-1 induction reduced atherosclerosis. It was also reported that HO-1 induction improved the cardiac function and postinfarction survival in animal models of heart failure or myocardial infarction. Recently, we and others examined blood HO-1 levels in patients with atherosclerotic diseases, e.g., coronary artery disease (CAD) and peripheral artery disease (PAD). Taken together, these findings to date support the notion that HO-1 plays a protective role against the progression of atherosclerotic diseases. This review summarizes the roles of HO-1 in atherosclerosis and focuses on the clinical studies that examined the relationships between HO-1 levels and atherosclerotic diseases.

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Section: Ho-1 Expression In Patients With Atherosclerotic Diseasesmentioning

confidence: 99%

“…The whiskers represent the lowest and highest value in the 25th percentile minus 1.5 IQR and 75th percentile plus 1.5 IQR, respectively. (Modified from Kishimoto et al [25]).…”

Section: Figurementioning

confidence: 99%

The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases

Kishimoto

Kondo

Momiyama

2019

IJMS

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“…The pivotal role of HO-1 is also suggested by Cheng et al, who have reported the HO-1 induction reverses plaque progression from a vulnerable to a more stable phenotype [77], which might be mediated by heme catabolism by-products. In addition, plasma HO-1 levels are higher in patients with carotid plaques compared to healthy subjects, which probably indicates a possible protective response against carotid atherosclerosis [78].…”

Section: Atherosclerosismentioning

confidence: 99%

Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress—A New Insight into the Pathophysiology of Vascular Diseases

Gáll

Balla

2019

IJMS

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The prevalence of vascular disorders continues to rise worldwide. Parallel with that, new pathophysiological pathways have been discovered, providing possible remedies for prevention and therapy in vascular diseases. Growing evidence suggests that endoplasmic reticulum (ER) stress is involved in a number of vasculopathies, including atherosclerosis, vascular brain events, and diabetes. Heme, which is released from hemoglobin or other heme proteins, triggers various pathophysiological consequence, including heme stress as well as ER stress. The potentially toxic free heme is converted by heme oxygenases (HOs) into carbon monoxide (CO), iron, and biliverdin (BV), the latter of which is reduced to bilirubin (BR). Redox-active iron is oxidized and stored by ferritin, an iron sequestering protein which exhibits ferroxidase activity. In recent years, CO, BV, and BR have been shown to control cellular processes such as inflammation, apoptosis, and antioxidant defense. This review covers our current knowledge about how heme induced endoplasmic reticulum stress (HIERS) participates in the pathogenesis of vascular disorders and highlights recent discoveries in the molecular mechanisms of HO-mediated cytoprotection in heme stress and ER stress, as well as crosstalk between ER stress and HO-1. Furthermore, we focus on the translational potential of HIERS and heme oxygenase-1 (HO-1) in atherosclerosis, diabetes mellitus, and brain hemorrhage.

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“…The association between the presence of atherosclerosis or CAD and serum HO-1 levels has been investigated in previous studies. Kishimoto et al [16] found that patients without carotid plaques had significantly lower plasma HO-1 levels than the ones with carotid plaques (median 0.44 vs. 0.56 ng/mL, p < 0.05). Moreover, regression analysis showed that an HO-1 level >0.50 ng/mL was independently associated with the presence of carotid plaques (odds ratio: 2.33, 95% CI: 1.15–4.75, p < 0.025).…”

Section: Discussionmentioning

confidence: 99%

The Association between Serum Heme Oxygenase-1 Levels and Coronary SYNTAX Score

et al. 2021

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Aim: The relationship between heme oxygenase-1 (HO-1) levels and atherosclerosis was investigated in multiple studies. The aim of this study was to establish the relationship between HO-1 levels and coronary SYNergy between percutaneous coronary intervention with TAXus and Cardiac Surgery (SYNTAX) score in patients with stable coronary artery disease (CAD). Methods: Patients who had been planned to undergo invasive coronary angiography due to a suspected CAD, between the dates of September and December 2019, were included in the study. Serum HO-1 levels were measured from peripheral venous blood. The SYNTAX score was calculated using standard coronary angiography images. Regression analysis was performed to establish the relationship between HO-1 levels and the SYNTAX score. Results: In total, 137 patients were included. The median age was 63 years (IQR: 15), and most of the patients were male (75.2%). The median HO-1 level was 1.44 (IQR: 0.88) ng/mL, and the median SYNTAX score was 6 (IQR: 13). Regression analysis showed that HO-1 is the single most important variable associated with the SYNTAX score (HO-1 levels from 1.01 to 1.87 ng/mL, OR: 6.77, 95% confidence interval 5.18–8.36, p < 0.0001). Conclusion: In this study, serum HO-1 levels were significantly associated with the coronary SYNTAX score.

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Plasma Heme Oxygenase-1 Levels and Carotid Atherosclerosis

Cited by 17 publications

References 13 publications

The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases

The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases

Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress—A New Insight into the Pathophysiology of Vascular Diseases

The Association between Serum Heme Oxygenase-1 Levels and Coronary SYNTAX Score

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