2023
DOI: 10.1016/j.heliyon.2023.e17193
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Cavin-2 loss exacerbates hypoxia-induced pulmonary hypertension with excessive eNOS phosphorylation and protein nitration

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Cited by 6 publications
(1 citation statement)
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“…We observed interaction of age and ischemia for Cavin2 in the aging male myocardium more specifically repression of Cavin2 in post-ischemic middle-aged hearts. Though yet to be shown in the heart (specifically in cardiomyocytes), Cavin-2 reduction via knockdown has been shown to result in detrimental outcomes in lung models of I-R injury, conversely Cavin2 -overexpresison has been found to reduce production of inflammatory factors and oxidative stress injury (Kasahara et al, 2023; Tang et al, 2022). Similarly a recent report suggests that fibroblast-specific Cavin-2-deficiency attenuates cardiac fibrosis resulting in the suppression of heart failure (Higuchi et al 2024).…”
Section: Discussionmentioning
confidence: 99%
“…We observed interaction of age and ischemia for Cavin2 in the aging male myocardium more specifically repression of Cavin2 in post-ischemic middle-aged hearts. Though yet to be shown in the heart (specifically in cardiomyocytes), Cavin-2 reduction via knockdown has been shown to result in detrimental outcomes in lung models of I-R injury, conversely Cavin2 -overexpresison has been found to reduce production of inflammatory factors and oxidative stress injury (Kasahara et al, 2023; Tang et al, 2022). Similarly a recent report suggests that fibroblast-specific Cavin-2-deficiency attenuates cardiac fibrosis resulting in the suppression of heart failure (Higuchi et al 2024).…”
Section: Discussionmentioning
confidence: 99%