β-Nicotinamide Mononucleotide protects against endotoxemia-induced myocardial injury through Sirt5-dependent desuccinylation of succinate dehydrogenase.

Tao H, Dong Q, Long Y, Liu L, Qin S, Wang Y

European journal of pharmacology16 Jan 2026

PMID41548684DOI10.1016/j.ejphar.2026.178562PepBankPUB-41548684

Publisher page PubMedAsk about this study

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 study16

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice, NMN gradually increased myocardial NAD to saturation, peaking at 14 days.
In plain wordsIn mice, NMN increased heart NAD levels, with a peak at 14 days.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseMyocardial NAD levels
Study
mousen: not reported in source
mice receiving NMN
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Myocardial NAD⁺ levels gradually increased to a saturation level (peaking at 14 days), with no obvious adverse effects.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868401
02AnimalAnimal study (in vivo)Safety outcome
In mice receiving NMN, the study reported no obvious adverse effects.
In plain wordsIn mice receiving NMN, the study reported no obvious adverse effects.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
No significant changeObvious adverse effects
Study
mousen: not reported in source
mice receiving NMN
Outcome group
Adverse events · Whole body
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Myocardial NAD⁺ levels gradually increased to a saturation level (peaking at 14 days), with no obvious adverse effects.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868402
03AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced myocardial injury, NMN significantly improved survival rates.
In plain wordsIn mice with inflammatory heart injury, NMN improved survival.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseSurvival
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Mortality · Whole body
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
In LPS-induced myocardial injury, NMN supplementation significantly improved survival rates, reduced serum cardiac troponin I (cTnI), enhanced cardiac function, restored ATP production, downregulated pro-inflammatory cytokines, and alleviated oxidative damage.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868403
04AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced myocardial injury, NMN reduced serum cardiac troponin I.
In plain wordsIn mice with inflammatory heart injury, NMN reduced a blood marker of heart damage.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSerum cardiac troponin I
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Heart function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
In LPS-induced myocardial injury, NMN supplementation significantly improved survival rates, reduced serum cardiac troponin I (cTnI), enhanced cardiac function, restored ATP production, downregulated pro-inflammatory cytokines, and alleviated oxidative damage.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868404
05AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced myocardial injury, NMN enhanced cardiac function.
In plain wordsIn mice with inflammatory heart injury, NMN improved heart function.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
MixedCardiac function
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Heart function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
In LPS-induced myocardial injury, NMN supplementation significantly improved survival rates, reduced serum cardiac troponin I (cTnI), enhanced cardiac function, restored ATP production, downregulated pro-inflammatory cytokines, and alleviated oxidative damage.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868405
06AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced myocardial injury, NMN restored ATP production.
In plain wordsIn mice with inflammatory heart injury, NMN restored cellular energy production.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseATP production
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
In LPS-induced myocardial injury, NMN supplementation significantly improved survival rates, reduced serum cardiac troponin I (cTnI), enhanced cardiac function, restored ATP production, downregulated pro-inflammatory cytokines, and alleviated oxidative damage.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868406
07AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced myocardial injury, NMN downregulated pro-inflammatory cytokines.
In plain wordsIn mice with inflammatory heart injury, NMN reduced inflammatory signaling proteins.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreasePro-inflammatory cytokines
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Inflammation markers · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
In LPS-induced myocardial injury, NMN supplementation significantly improved survival rates, reduced serum cardiac troponin I (cTnI), enhanced cardiac function, restored ATP production, downregulated pro-inflammatory cytokines, and alleviated oxidative damage.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868407
08AnimalAnimal study (in vivo)Efficacy outcome
In mice with LPS-induced myocardial injury, NMN alleviated oxidative damage.
In plain wordsIn mice with inflammatory heart injury, NMN reduced oxidative damage.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseOxidative damage
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Heart function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
In LPS-induced myocardial injury, NMN supplementation significantly improved survival rates, reduced serum cardiac troponin I (cTnI), enhanced cardiac function, restored ATP production, downregulated pro-inflammatory cytokines, and alleviated oxidative damage.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868408
09AnimalAnimal study (in vivo)Mechanism
In mice with endotoxemic myocardial injury, NMN corrected aberrant SDH catalytic function.
In plain wordsIn mice with inflammatory heart injury, NMN corrected abnormal SDH enzyme function.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
MixedSDH catalytic function
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
We further discovered that NMN corrected the aberrant catalytic function of SDH, reduced succinate accumulation, and increased fumarate levels.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868409
10AnimalAnimal study (in vivo)Mechanism
In mice with endotoxemic myocardial injury, NMN reduced succinate accumulation.
In plain wordsIn mice with inflammatory heart injury, NMN reduced succinate accumulation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSuccinate accumulation
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
We further discovered that NMN corrected the aberrant catalytic function of SDH, reduced succinate accumulation, and increased fumarate levels.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868410
11AnimalAnimal study (in vivo)Mechanism
In mice with endotoxemic myocardial injury, NMN increased fumarate levels.
In plain wordsIn mice with inflammatory heart injury, NMN increased fumarate levels.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseFumarate levels
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
We further discovered that NMN corrected the aberrant catalytic function of SDH, reduced succinate accumulation, and increased fumarate levels.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868411
12AnimalAnimal study (in vivo)Mechanism
In mice with endotoxemic myocardial injury, NMN reduced SDH succinylation.
In plain wordsIn mice with inflammatory heart injury, NMN reduced succinylation of the SDH enzyme.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSDH succinylation
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Mechanistically, NMN supplementation specifically reduced SDH succinylation (but not acetylation) and promoted the binding of Sirt5 to SDH.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868412
13AnimalAnimal study (in vivo)Mechanism
In mice with endotoxemic myocardial injury, NMN did not reduce SDH acetylation.
In plain wordsIn mice with inflammatory heart injury, NMN did not reduce acetylation of the SDH enzyme.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
No significant changeSDH acetylation
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Mechanistically, NMN supplementation specifically reduced SDH succinylation (but not acetylation) and promoted the binding of Sirt5 to SDH.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868413
14AnimalAnimal study (in vivo)Mechanism
In mice with endotoxemic myocardial injury, NMN promoted Sirt5 binding to SDH.
In plain wordsIn mice with inflammatory heart injury, NMN increased Sirt5 binding to SDH.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseSirt5 binding to SDH
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
500 mg/kg · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Mechanistically, NMN supplementation specifically reduced SDH succinylation (but not acetylation) and promoted the binding of Sirt5 to SDH.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
Report a problemFND-4154868414

Studies that did not test the peptide alone2

In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NMN (nicotinamide mononucleotide).

15AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice, cardiomyocyte-specific Sirt5 knockdown attenuated NMN-associated SDH desuccinylation.
In plain wordsIn mice, reducing the Sirt5 gene weakened NMN-associated removal of succinyl groups from SDH.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSirt5 dependence of SDH desuccinylation
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
After cardiomyocyte-specific knockdown of Sirt5, the protective effects of NMN on SDH desuccinylation and myocardial protection were significantly attenuated.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4154868415
16AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In mice, cardiomyocyte-specific Sirt5 knockdown attenuated NMN-associated myocardial protection.
In plain wordsIn mice, reducing the Sirt5 gene weakened NMN-associated heart protection.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSirt5 dependence of myocardial protection
Study
mousen: not reported in source
LPS-induced myocardial injury
Outcome group
Heart function · Cardiovascular
Source sentences
Summary
After cardiomyocyte-specific knockdown of Sirt5, the protective effects of NMN on SDH desuccinylation and myocardial protection were significantly attenuated.
1 context sentence(design, population, supporting numbers)
Summary · context
Mice were intraperitoneally administered NMN (500 mg/kg) for 1, 7, 14, 21, and 28 consecutive days.
In this study, NMN (nicotinamide mononucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NMN (nicotinamide mononucleotide).
Report a problemFND-4154868416

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.

Version 2Current
21 Oct 2026, 15:58 UTC
Study results updated
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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