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Study · Animal study (in vivo) · rat · 2020

13 results

NAD+ administration decreases microvascular damage following cardiac ischemia/reperfusion by restoring autophagic flux.

Zhang YJ, Zhang M, Zhao X, Shi K, Ye M, Tian J, Guan S, Ying W, Qu X

Basic research in cardiology10 Aug 2020Cited by 52 (Europe PMC)

PMID32778948 (opens in a new tab)DOI10.1007/s00395-020-0817-z (opens in a new tab)PepBankPUB-32778948
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study13

13 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia/reperfusion, NAD+ attenuated reduced regional blood perfusion.

    In plain wordsIn rats, NAD+ reduced the loss of regional blood perfusion after myocardial ischemia/reperfusion.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseRegional blood perfusion
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia/reperfusion, NAD+ attenuated decreased microvessel density.

    In plain wordsIn rats, NAD+ reduced the loss of microvessel density after myocardial ischemia/reperfusion.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseMicrovessel density
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia/reperfusion, NAD+ attenuated decreased microvessel integrity.

    In plain wordsIn rats, NAD+ reduced the loss of microvessel integrity after myocardial ischemia/reperfusion.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseMicrovessel integrity
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia/reperfusion, NAD+ attenuated coronary microvascular endothelial cell injury.

    In plain wordsIn rats, NAD+ reduced coronary microvascular endothelial cell injury after myocardial ischemia/reperfusion.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCMEC injury
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In rat CMECs exposed to ischemia/reperfusion, NAD+ restored impaired autophagic flux.

    In plain wordsIn rats, NAD+ restored impaired autophagic flux in coronary microvascular endothelial cells.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseAutophagic flux
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD+ significantly rescued the impaired autophagic flux and cell apoptosis that was induced by I/R in rat CMECs
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In rat CMECs exposed to ischemia/reperfusion, NAD+ rescued induced cell apoptosis.

    In plain wordsIn rats, NAD+ reduced induced apoptosis in coronary microvascular endothelial cells.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCell apoptosis
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD+ significantly rescued the impaired autophagic flux and cell apoptosis that was induced by I/R in rat CMECs
  7. 07AnimalAnimal study (in vivo)Mechanism

    In cells exposed to rat myocardial ischemia/reperfusion, NAD+ induced TFEB activation.

    In plain wordsIn rats, NAD+ increased TFEB activation in cells exposed to myocardial ischemia/reperfusion.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseTFEB activation
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In cells exposed to rat myocardial ischemia/reperfusion, NAD+ attenuated lysosomal dysfunction.

    In plain wordsIn rats, NAD+ reduced lysosomal dysfunction in cells exposed to myocardial ischemia/reperfusion.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseLysosomal dysfunction
    Study

    ratn: not reported in source

    Myocardial ischemia/reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells.
  9. 09LabIn vitro (cells)Mechanism

    In primary cultured CMECs exposed to hypoxia/reoxygenation, NAD+ restored autophagic flux, particularly lysosomal autophagy.

    In plain wordsIn cells, NAD+ restored autophagic flux after hypoxia/reoxygenation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseAutophagic flux
    Study

    ratn: not reported in source

    Primary cultured CMECs under hypoxia/reoxygenation
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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
  10. 10LabIn vitro (cells)Efficacy outcome

    In cultured rat CMECs, NAD+ rescued induced cell apoptosis in the in vitro ischemia/reperfusion experiments.

    In plain wordsIn cells, NAD+ reduced induced apoptosis in the rat coronary microvascular endothelial cell experiments.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCell apoptosis
    Study

    ratn: not reported in source

    Primary cultured rat CMECs
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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
  11. 11LabIn vitro (cells)Mechanism

    In CMECs exposed to hypoxia/reoxygenation, NAD+ induced TFEB activation.

    In plain wordsIn cells exposed to hypoxia/reoxygenation, NAD+ increased TFEB activation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseTFEB activation
    Study

    ratn: not reported in source

    Primary cultured CMECs under hypoxia/reoxygenation
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells.
  12. 12LabIn vitro (cells)Mechanism

    In CMECs exposed to hypoxia/reoxygenation, NAD+ attenuated lysosomal dysfunction.

    In plain wordsIn cells exposed to hypoxia/reoxygenation, NAD+ reduced lysosomal dysfunction.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseLysosomal dysfunction
    Study

    ratn: not reported in source

    Primary cultured CMECs under hypoxia/reoxygenation
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD+ treatment markedly induced transcription factor EB (TFEB) activation and attenuated lysosomal dysfunction in the I/R or HR-exposed cells.
  13. 13LabIn vitro (cells)Efficacy outcome

    In cultured rat CMECs exposed to hypoxia/reoxygenation, NAD+ had a protective effect partly mediated by restored autophagic flux.

    In plain wordsIn cells exposed to hypoxia/reoxygenation, NAD+ protection appeared partly mediated by restored autophagic flux.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseCMEC protection under hypoxia/reoxygenation
    Study

    ratn: not reported in source

    Primary cultured CMECs under hypoxia/reoxygenation
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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