NAD+ administration decreases microvascular damage following cardiac ischemia/reperfusion by restoring autophagic flux
Microvascular damage is a key pathological change in myocardial ischemia/reperfusion (I/R) injury. Using a rat model of myocardial I/R, our current study has provided the first evidence that nicotinamide adenine dinucleotide (NAD+) administration can significantly attenuate myocardial I/R-induced microvascular damage, including reduced regional blood perfusion, decreased microvessel density and integrity, and coronary microvascular endothelial cells (CMECs) injury. In studies with primary cultured CMECs under hypoxia/reoxygenation (HR) and a rat model of I/R, our results suggested that the protective effect of NAD+ on CMECs exposed to HR or I/R is at least partially mediated by the NAD+-induced restoration of autophagic flux, especially lysosomal autophagy: NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells. Collectively, our study has provided the first in vivo and in vitro evidence that NAD+ significantly rescued the impaired autophagic flux and cell apoptosis that was induced by I/R in rat CMECs, which is mediated in part through the action of TFEB-mediated lysosomal autophagy.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:115 |
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Enthalten in: |
Basic research in cardiology - 115(2020), 5 vom: 10. Aug., Seite 57 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Zhang, You-Jun [VerfasserIn] |
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Links: |
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Themen: |
0U46U6E8UK |
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Anmerkungen: |
Date Completed 25.06.2021 Date Revised 25.06.2021 published: Electronic Citation Status MEDLINE |
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doi: |
10.1007/s00395-020-0817-z |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM313538344 |
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520 | |a Microvascular damage is a key pathological change in myocardial ischemia/reperfusion (I/R) injury. Using a rat model of myocardial I/R, our current study has provided the first evidence that nicotinamide adenine dinucleotide (NAD+) administration can significantly attenuate myocardial I/R-induced microvascular damage, including reduced regional blood perfusion, decreased microvessel density and integrity, and coronary microvascular endothelial cells (CMECs) injury. In studies with primary cultured CMECs under hypoxia/reoxygenation (HR) and a rat model of I/R, our results suggested that the protective effect of NAD+ on CMECs exposed to HR or I/R is at least partially mediated by the NAD+-induced restoration of autophagic flux, especially lysosomal autophagy: NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells. Collectively, our study has provided the first in vivo and in vitro evidence that NAD+ significantly rescued the impaired autophagic flux and cell apoptosis that was induced by I/R in rat CMECs, which is mediated in part through the action of TFEB-mediated lysosomal autophagy | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Autophagic flux | |
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700 | 1 | |a Shi, Kailei |e verfasserin |4 aut | |
700 | 1 | |a Ye, Maoqing |e verfasserin |4 aut | |
700 | 1 | |a Tian, Jiawen |e verfasserin |4 aut | |
700 | 1 | |a Guan, Shaofeng |e verfasserin |4 aut | |
700 | 1 | |a Ying, Weihai |e verfasserin |4 aut | |
700 | 1 | |a Qu, Xinkai |e verfasserin |4 aut | |
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