$ NAD^{+} $ administration decreases microvascular damage following cardiac ischemia/reperfusion by restoring autophagic flux
Abstract 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. |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhang, You-Jun [VerfasserIn] |
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| Links: |
Volltext [lizenzpflichtig] |
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| BKL: | |
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| Themen: |
Autophagic flux |
| doi: |
10.1007/s00395-020-0817-z |
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| funding: |
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| Förderinstitution / Projekttitel: |
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SPR040613348 |
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| 520 | |a Abstract 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. | ||
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| 700 | 1 | |a Zhao, Xiaona |e verfasserin |4 aut | |
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| 700 | 1 | |a Ye, Maoqing |e verfasserin |4 aut | |
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| 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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