Vascular smooth muscle cells activate PI3K/Akt pathway to attenuate myocardial ischemia/reperfusion-induced apoptosis and autophagy by secreting bFGF

Ye, Guohong; Fu, Qiang; Jiang, Liangjun; Li, Zhiliang

doi:10.1016/j.biopha.2018.05.113

Cited by 45 publications

(34 citation statements)

References 26 publications

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“…Moreover, Guohong Ye et al found that VSMCs secrete bFGF to the medium, and then activate the PI3K/AKT signaling pathway by binding to cardiomyocyte FGFR1 in the hypoxia state, thereby weakening the apoptosis and autophagy of myocardial I/R [93]. STIM1 plays an important role in regulating calcium signaling pathways in different cell types, including SMCs [94].…”

Section: Smcs In MImentioning

confidence: 99%

Role of smooth muscle cells in Cardiovascular Disease

et al. 2020

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Normally, smooth muscle cells (SMCs) are localized in the tunica media of the vasculature, where they take responsibility for vascular contraction and extracellular matrix (ECM) generation. SMCs also play a significant role in obedience and elastic rebound of the artery in response to the haemodynamic condition. However, under pathological or stressed conditions, phenotype switching from contractile to synthetic state or other cell types will occur in SMCs to positively or negatively contribute to disease progression. Various studies demonstrated that functional changes of SMCs are implicated in several cardiovascular diseases. In this review, we present the function of vascular SMCs (VSMCs) and the involved molecular mechanisms about phenotype switching, and summarize the roles of SMCs in atherosclerosis, hypertension, arterial aneurysms and myocardial infarction, hoping to obtain potential therapeutic targets against cardiovascular disease in the clinical practices.

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Section: Smcs In MImentioning

confidence: 99%

Role of smooth muscle cells in Cardiovascular Disease

et al. 2020

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“…PI3K/Akt is a well-known signalling pathway involved in myocardial protection (Hausenloy and Yellon 2004 ). Several studies have shown that the activation of the PI3K/Akt signalling pathway attenuated myocardial I/R injury by inhibiting the inflammatory response, endoplasmic reticulum stress-regulated apoptosis and autophagy (Xu et al 2018 ; Ye et al 2018 ; Yu et al 2019 ). However, it was unclear whether the PI3K/Akt pathway mediates the cardioprotective effects of Sal B.…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway

Liu

Qiu

et al. 2019

Naunyn-Schmiedeberg's Arch Pharmacol

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Salvianolic acid B (Sal B) has a significant protective effect on myocardial ischaemia-reperfusion (I/R) injury. Therefore, the aims of this study were to determine the effects of Sal B on myocardial ischaemic-reperfusion (I/R) injury in rats and to explore whether its underlying mechanism of cardioprotection occurs through activating the expression of the phosphoinositide 3-kinase/ protein, kinase B (PI3K/Akt) and inhibiting the expression of high mobility group protein 1 (HMGB1). Ninety Sprague-Dawley rats were randomized into five groups: group 1 (sham-operated), group 2 (myocardial I/R), group 3 (low dose of Sal B+I/R), group 4 (high dose of Sal B+I/R), and group 5 (high dose of Sal B+I/R+LY294002, which is a specific PI3k inhibitor). All I/R rats received 30 min myocardial ischaemia followed by 24-h reperfusion. Cardiac function, infarct size, myocardial injury marker levels, inflammatory response and cardiomyocyte apoptosis as well as Bcl-2, Bax, P-Akt, HMGB1 and TLR4 expression were measured. In the current study, Sal B significantly ameliorated myocardial I/R injury in a dose-dependent manner, ameliorated cardiac function, reduced myocardial infarction size, decreased myocardial injury marker expression, decreased inflammatory responses, reduced apoptosis, activated PI3K/Akt expression and inhibited HMGB1 expression. However, all effects of Sal B were significantly reversed by LY294002. Overall, the present study indicated that Sal B attenuated myocardial I/R injury by activating PI3K/Akt and inhibiting the release of HMGB1 in rats.

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“…Myocardial infarction has been a leading cause of morbidity and mortality worldwide [1,2]. Percutaneous coronary intervention could effectively restore blood supply to ischemic myocardium, then reduce myocardial infarct size and improve prognosis [3,4].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of P300/CBP-Associated Factor Attenuates Myocardial Ischemia-Reperfusion Injury Via Inhibiting Autophagy

Qiu¹,

Xu²,

Xia³

et al. 2020

Int. J. Med. Sci.

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Cardiomyocyte autophagy plays an important role in myocardial ischemia-reperfusion injury (MIRI). P300/CBP-associated factor (PCAF) was involved in the regulation of autophagy. However, the role of PCAF in MIRI is currently unknown. This study was to investigate whether downregulation of PCAF attenuate MIRI. The results showed that the expression of PCAF was significantly increased in MIRI in vivo and in vitro. Downregulation of PCAF not only inhibited autophagy and damage of H9c2 cells induced by hypoxia-reoxygenation, but also reduced autophagy and myocardial infarct size during myocardial ischemia-reperfusion in rats. In addition, downregulation of PCAF promoted activation of PI3K/Akt/mTOR signaling pathway in cardiomyocytes during hypoxia-reoxygenation. Wortmannin, a PI3K/Akt inhibitor, could abrogate the effects of downregulation of PCAF on cardiomyocytes autophagy. These results demonstrated that downregulation of PCAF alleviated MIRI by inhibiting cardiomyocyte autophagy through PI3K/Akt/mTOR signaling pathway. Thus, PCAF may be a potential target for prevention and treatment of MIRI.

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Vascular smooth muscle cells activate PI3K/Akt pathway to attenuate myocardial ischemia/reperfusion-induced apoptosis and autophagy by secreting bFGF

Cited by 45 publications

References 26 publications

Role of smooth muscle cells in Cardiovascular Disease

Role of smooth muscle cells in Cardiovascular Disease

Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway

Downregulation of P300/CBP-Associated Factor Attenuates Myocardial Ischemia-Reperfusion Injury Via Inhibiting Autophagy

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