Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Xia, Weiyi; Zhang, Miao; Liu, Chang; Wang, Sheng; Xu, Aimin; Xia, Zhengyuan; Pang, Lei; Cai, Yin

doi:10.1016/j.lfs.2024.122594

Life Sciences

2024

DOI: 10.1016/j.lfs.2024.122594

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Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Weiyi Xia,

Miao Zhang,

Chang Liu

et al.

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Cited by 3 publications

References 262 publications

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From exosomes to mitochondria and myocardial infarction: Molecular insight and therapeutic challenge

Liu,

Zhang,

Long

et al. 2024

Pharmacological Research

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From exosomes to mitochondria and myocardial infarction: Molecular insight and therapeutic challenge

Liu,

Zhang,

Long

et al. 2024

Pharmacological Research

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Redox Homeostasis and Molecular Biomarkers in Precision Therapy for Cardiovascular Diseases

Drăgoi,

Diaconu,

Nicolae

et al. 2024

Antioxidants

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Precision medicine is envisioned as the future of cardiovascular healthcare, offering a more tailored and effective method for managing cardiovascular diseases compared to the traditional one-size-fits-all approaches. The complex role of oxidative stress in chronic diseases within the framework of precision medicine was carefully explored, delving into the cellular redox status and its critical involvement in the pathophysiological complexity of cardiovascular diseases (CVDs). The review outlines the mechanisms of reactive oxygen species generation and the function of antioxidants in maintaining redox balance. It emphasizes the elevated reactive oxygen species concentrations observed in heart failure and their detrimental impact on cardiovascular health. Various sources of ROS within the cardiovascular system are examined, including mitochondrial dysfunction, which contributes to oxidative stress and mitochondrial DNA degradation. The article also addresses oxidative stress’s role in myocardial remodeling, a process pivotal to the progression of heart diseases. By integrating these aspects, the review underscores the importance of redox homeostasis and identifies molecular biomarkers that can enhance precision therapy for CVDs. The insights provided aim to pave the way for targeted therapeutic strategies that mitigate oxidative stress, thereby improving patient outcomes in cardiovascular medicine.

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Replicative Endothelial Cell Senescence May Lead to Endothelial Dysfunction by Increasing the BH2/BH4 Ratio Induced by Oxidative Stress, Reducing BH4 Availability, and Decreasing the Expression of eNOS

Hernandez-Navarro,

Botana,

Diez-Mata

et al. 2024

IJMS

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Vascular aging is associated with the development of cardiovascular complications, in which endothelial cell senescence (ES) may play a critical role. Nitric oxide (NO) prevents human ES through inhibition of oxidative stress, and inflammatory signaling by mechanisms yet to be elucidated. Endothelial cells undergo an irreversible growth arrest and alter their functional state after a finite number of divisions, a phenomenon called replicative senescence. We assessed the contribution of NO during replicative senescence of human aortic (HAEC) and coronary (CAEC) endothelial cells, in which accumulation of the senescence marker SA-β-Gal was quantified by β-galactosidase staining on cultured cells. We found a negative correlation in passaged cell cultures from P0 to P12, between a reduction in NO production with increased ES and the formation of reactive oxygen (ROS) and nitrogen (ONOO−) species, indicative of oxidative and nitrosative stress. The effect of ES was evidenced by reduced expression of endothelial Nitric Oxide Synthase (eNOS), Interleukin Linked Kinase (ILK), and Heat shock protein 90 (Hsp90), alongside a significant increase in the BH2/BH4 ratio, inducing the uncoupling of eNOS, favoring the production of superoxide and peroxynitrite species, and fostering an inflammatory environment, as confirmed by the levels of Cyclophilin A (CypA) and its receptor Extracellular Matrix Metalloprotease Inducer (EMMPRIN). NO prevents ES by preventing the uncoupling of eNOS, in which oxidation of BH4, which plays a key role in eNOS producing NO, may play a critical role in launching the release of free radical species, triggering an aging-related inflammatory response.

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Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Cited by 3 publications

References 262 publications

From exosomes to mitochondria and myocardial infarction: Molecular insight and therapeutic challenge

From exosomes to mitochondria and myocardial infarction: Molecular insight and therapeutic challenge

Redox Homeostasis and Molecular Biomarkers in Precision Therapy for Cardiovascular Diseases

Replicative Endothelial Cell Senescence May Lead to Endothelial Dysfunction by Increasing the BH2/BH4 Ratio Induced by Oxidative Stress, Reducing BH4 Availability, and Decreasing the Expression of eNOS

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