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Study · Animal study (in vivo) · mouse · 2026

3 results

Administration of Nicotinamide Mononucleotide Mitigates the HIV Nef-Induced Metabolic and Pathological Changes in the Heart.

Kondrachuk O, Nakhungu E, Ogundipe G, Tailor N, Ciccone P, Hong K, Gadiraju A, Kimura Y, Zi A, Yusuf S, Alkousa A, Nguyen S and 4 more

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Rajkumar R, Do J, Rappaport J, Gupta MK

Cells1 Mar 2026Cited by 1 (Europe PMC)

PMID41827877 (opens in a new tab)PMCIDPMC12984467 (opens in a new tab)DOI10.3390/cells15050444 (opens in a new tab)PepBankPUB-41827877
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Summary

Due to the application of antiretroviral therapy, HIV has become a manageable chronic disease, and people living with HIV/AIDS (PLWHA) experience several comorbidities, including cardiovascular disease. Although antiretroviral therapy suppresses the viral load to an undetectable level, HIV proteins can still be detected in the circulation and in different organs. In our previous study, we found that the expression of the Nef protein causes cardiac dysfunction and heart failure in a transgenic mouse model. We also observed inhibition of autophagy along with the upregulation of the senescence marker Bcl2. To further understand the metabolic changes related to Nef in cardiac tissue, we examined nicotinamide adenine dinucleotide (NAD) metabolism in the heart. Our metabolic study with cardiac tissue revealed that Nef expression decreases NAD+ levels in the heart. Additionally, we explored whether replenishing cellular NAD+ could be a potential therapeutic target for HIV-associated cardiovascular disease. Interestingly, our study found that NMN treatment can improve cellular autophagy, decrease the senescence marker Bcl2, and reduce fibrosis in the heart. Overall, our study suggests that NMN could serve as a promising therapeutic molecule for the treatment of HIV-associated cardiovascular comorbidities.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In the Nef cardiac disease model, NMN improved cellular autophagy.

    In plain wordsIn mice with a Nef heart disease model, NMN improved cellular recycling in the heart.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseCardiac autophagy
    Study

    mousen: not reported in source

    Nef transgenic mouse model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Interestingly, our study found that NMN treatment can improve cellular autophagy, decrease the senescence marker Bcl2, and reduce fibrosis in the heart.
    1 context sentence
    Summary · context
    In our previous study, we found that the expression of the Nef protein causes cardiac dysfunction and heart failure in a transgenic mouse model.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In the Nef cardiac disease model, NMN decreased the senescence marker Bcl2.

    In plain wordsIn mice with a Nef heart disease model, NMN reduced the cell-aging marker Bcl2.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseBcl2 senescence marker
    Study

    mousen: not reported in source

    Nef transgenic mouse model
    Outcome group
    Aging markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Interestingly, our study found that NMN treatment can improve cellular autophagy, decrease the senescence marker Bcl2, and reduce fibrosis in the heart.
    1 context sentence
    Summary · context
    In our previous study, we found that the expression of the Nef protein causes cardiac dysfunction and heart failure in a transgenic mouse model.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In the Nef cardiac disease model, NMN reduced cardiac fibrosis.

    In plain wordsIn mice with a Nef heart disease model, NMN reduced heart scarring.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCardiac fibrosis
    Study

    mousen: not reported in source

    Nef transgenic mouse model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Interestingly, our study found that NMN treatment can improve cellular autophagy, decrease the senescence marker Bcl2, and reduce fibrosis in the heart.
    1 context sentence
    Summary · context
    In our previous study, we found that the expression of the Nef protein causes cardiac dysfunction and heart failure in a transgenic mouse model.

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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