Senkyunolide I ameliorates thoracic aortic aneurysm and dissection in mice via inhibiting the oxidative stress and apoptosis of endothelial cells

Zhao, Kaiwen; Zhu, Hongqiao; He, Xiaomin; Du, Pengcheng; Liang, Taiping; Sun, Yudong; Jing, Zaiping; Zhou, Jian

doi:10.1016/j.bbadis.2023.166819

Cited by 6 publications

(2 citation statements)

References 27 publications

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“…Indeed, many recent studies support this notion (Table S1). Such therapies include treatments with dexamethasone [27,108], folic acid [81], metformin [39], melatonin [31], digoxin [90], oltipraz [33], TEPP-46 (activator of glycolytic enzyme pyruvate kinase M2) [32], cordycepin [65], myriocin [36], senkyunolide I [187], allopurinol [188], angiotensin 1-7 [48], macrophage inhibitors [34], and angiogenic factor with G-patch and FHA domains 1 [40].…”

Section: Inhibition Of Inflammationmentioning

confidence: 99%

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm

Wang,

Panicker,

Anesi

et al. 2024

IJMS

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Thoracic aortic aneurysm (TAA) has a prevalence of 0.16–0.34% and an incidence of 7.6 per 100,000 person-years, accounting for 1–2% of all deaths in Western countries. Currently, no effective pharmacological therapies have been identified to slow TAA development and prevent TAA rupture. Large TAAs are treated with open surgical repair and less invasive thoracic endovascular aortic repair, both of which have high perioperative mortality risk. Therefore, there is an urgent medical need to identify the cellular and molecular mechanisms underlying TAA development and rupture to develop new therapies. In this review, we summarize animal TAA models including recent developments in porcine and zebrafish models: porcine models can assess new therapeutic devices or intervention strategies in a large mammal and zebrafish models can employ large-scale small-molecule suppressor screening in microwells. The second part of the review covers current views of TAA pathogenesis, derived from recent studies using these animal models, with a focus on the roles of the transforming growth factor-beta (TGFβ) pathway and the vascular smooth muscle cell (VSMC)-elastin-contractile unit. The last part discusses TAA treatment options as they emerge from recent preclinical studies.

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Section: Inhibition Of Inflammationmentioning

confidence: 99%

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm

Wang,

Panicker,

Anesi

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

“…Indeed, many recent studies support this notion (Table S6). Such therapies include treatments with dexamethasone [23,108], folic acid [81], metformin [35], melatonin [27], digoxin [90], oltipraz [29], TEPP-46 (activator of glycolytic enzyme pyruvate kinase M2) [28], cordycepin [65], myriocin [32], senkyunolide I [188], allopurinol [189], angiotensin 1-7 [44], macrophage inhibitors [30], and angiogenic factor with G-patch and FHA domains 1 [36].…”

Section: Inhibition Of Inflammationmentioning

confidence: 99%

Animal Models and Pathogenesis of Thoracic Aortic Aneurysm

Wang,

Panicker,

Anesi

et al. 2023

Preprint

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Thoracic aortic aneurysm (TAA) has a prevalence of 0.16%-0.34% and an incidence of 7.6 per 100,000 person-years, accounting for 1%-2% of all deaths in Western countries. Currently, no effective pharmacological therapies have been identified to slow TAA development and prevent TAA rupture. Large TAAs are treated with open surgical repair and less invasive thoracic endovascular aortic repair, both of which have high perioperative mortality risk. Therefore, there is an urgent medical need to identify the cellular and molecular mechanisms underlying TAA development and rupture to develop new therapies. In this review, we summarize animal TAA models including recent developments in porcine and zebrafish models: porcine models can assess new therapeutic devices or intervention strategies in a large mammal and zebrafish models can employ large-scale small-molecule suppressor screening in microwells. The second part of the review covers current views of TAA pathogenesis, with a focus on the roles of the transforming growth factor-beta (TGFβ) pathway and the vascular smooth muscle cell (VSMC)-elastin-contractile unit. The last part discusses TAA treatment options as they emerge from recent preclinical studies.

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Branched-chain amino acid catabolic defect in vascular smooth muscle cells drives thoracic aortic dissection via mTOR hyperactivation

Yu,

Huang,

Zhao

et al. 2024

Free Radical Biology and Medicine

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Senkyunolide I ameliorates thoracic aortic aneurysm and dissection in mice via inhibiting the oxidative stress and apoptosis of endothelial cells

Cited by 6 publications

References 27 publications

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm

Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm

Animal Models and Pathogenesis of Thoracic Aortic Aneurysm

Branched-chain amino acid catabolic defect in vascular smooth muscle cells drives thoracic aortic dissection via mTOR hyperactivation

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