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PEDF and 34‐mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO‐1 signalling in myocardial ischemia‐reperfusion injury
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PEDF and 34‐mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO‐1 signalling in myocardial ischemia‐reperfusion injury
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PEDF and 34‐mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO‐1 signalling in myocardial ischemia‐reperfusion injury
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Journal Article
PEDF and 34‐mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO‐1 signalling in myocardial ischemia‐reperfusion injury
2024
Overview
Myocardial ischemia‐reperfusion injury (MIRI) represents a critical pathology in acute myocardial infarction (AMI), which is characterized by high mortality and morbidity. Cardiac microvascular dysfunction contributes to MIRI, potentially culminating in heart failure (HF). Pigment epithelium‐derived factor (PEDF), which belongs to the non‐inhibitory serpin family, exhibits several physiological effects, including anti‐angiogenesis, anti‐inflammatory and antioxidant properties. Our study aims to explore the impact of PEDF and its functional peptide 34‐mer on both cardiac microvascular perfusion in MIRI rats and human cardiac microvascular endothelial cells (HCMECs) injury under hypoxia reoxygenation (HR). It has been shown that MIRI is accompanied by ferroptosis in HCMECs. Furthermore, we investigated the effect of PEDF and its 34‐mer, particularly regarding the Nrf2/HO‐1 signalling pathway. Our results demonstrated that PEDF 34‐mer significantly ameliorated cardiac microvascular dysfunction following MIRI. Additionally, they exhibited a notable suppression of ferroptosis in HCMECs, and these effects were mediated through activation of Nrf2/HO‐1 signalling. These findings highlight the therapeutic potential of PEDF and 34‐mer in alleviating microvascular dysfunction and MIRI. By enhancing cardiac microvascular perfusion and mitigating endothelial ferroptosis, PEDF and its derivative peptide represent promising candidates for the treatment of AMI.
Publisher
John Wiley and Sons Inc
Subject
/ Endothelial Cells - drug effects
/ Endothelial Cells - metabolism
/ Heme Oxygenase-1 - metabolism
/ Humans
/ Male
/ myocardial ischemia‐reperfusion injury
/ Myocardial Reperfusion Injury - drug therapy
/ Myocardial Reperfusion Injury - metabolism
/ Myocardial Reperfusion Injury - pathology
/ Nerve Growth Factors - metabolism
/ Nerve Growth Factors - pharmacology
/ NF-E2-Related Factor 2 - metabolism
/ Nrf2
/ Original
/ PEDF
/ Pigment Epithelium-Derived Factor
/ Rats
