Nicotinamide mononucleotide ameliorates acute lung injury by inducing mitonuclear protein imbalance and activating the UPR^mt.

Du SH, Shi J, Yu TY, Hu XX, He SM, Cao YY, Xie ZL, Liu SS, Li YT, Li N, Yu JB

Experimental biology and medicine (Maywood, N.J.)10 May 2022Cited by 6 (Europe PMC)

PMID35538652PMCIDPMC9379602DOI10.1177/15353702221094235PepBankPUB-35538652

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 study11

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

01AnimalAnimal study (in vivo)Mechanism
In endotoxemic mice, NMN pretreatment increased mitochondrial NAD+ levels.
In plain wordsIn mice, NMN pretreatment increased mitochondrial NAD+ during endotoxemia.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseMitochondrial NAD+
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Metabolic pathways and metabolomics · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
After pretreatment with NMN for 7 days, NAD⁺ levels in the mitochondrial, nucleus, and total intracellular were significantly increased in endotoxemia mice.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865201
02AnimalAnimal study (in vivo)Mechanism
In endotoxemic mice, NMN pretreatment increased nuclear NAD+ levels.
In plain wordsIn mice, NMN pretreatment increased nuclear NAD+ during endotoxemia.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseNuclear NAD+
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Metabolic pathways and metabolomics · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
After pretreatment with NMN for 7 days, NAD⁺ levels in the mitochondrial, nucleus, and total intracellular were significantly increased in endotoxemia mice.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865202
03AnimalAnimal study (in vivo)Mechanism
In endotoxemic mice, NMN pretreatment increased total intracellular NAD+ levels.
In plain wordsIn mice, NMN pretreatment increased total intracellular NAD+ during endotoxemia.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseTotal intracellular NAD+
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Metabolic pathways and metabolomics · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
After pretreatment with NMN for 7 days, NAD⁺ levels in the mitochondrial, nucleus, and total intracellular were significantly increased in endotoxemia mice.
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865203
04AnimalAnimal study (in vivo)Efficacy outcome
In mice with acute lung injury, NMN alleviated pathological lung injury.
In plain wordsIn mice, NMN reduced pathological lung injury.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLung pathological injury
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Lung injury and fibrosis · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
Moreover, supplementation of NMN alleviated lung pathologic injury, reduced ROS levels, increased MnSOD activities, mitigated mitochondrial dysfunction, ameliorated the defects in the nucleus morphology,
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865204
05AnimalAnimal study (in vivo)Mechanism
In mice with acute lung injury, NMN reduced ROS levels.
In plain wordsIn mice with lung injury, NMN reduced ROS levels.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseROS levels
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Oxidative stress · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
Moreover, supplementation of NMN alleviated lung pathologic injury, reduced ROS levels, increased MnSOD activities, mitigated mitochondrial dysfunction, ameliorated the defects in the nucleus morphology,
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865205
06AnimalAnimal study (in vivo)Mechanism
In mice with acute lung injury, NMN increased MnSOD activity.
In plain wordsIn mice with lung injury, NMN increased MnSOD activity.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseMnSOD activity
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Oxidative stress · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
Moreover, supplementation of NMN alleviated lung pathologic injury, reduced ROS levels, increased MnSOD activities, mitigated mitochondrial dysfunction, ameliorated the defects in the nucleus morphology,
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865206
07AnimalAnimal study (in vivo)Mechanism
In mice with acute lung injury, NMN mitigated mitochondrial dysfunction.
In plain wordsIn mice with lung injury, NMN reduced mitochondrial dysfunction.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseMitochondrial dysfunction
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Mitochondrial function · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
Moreover, supplementation of NMN alleviated lung pathologic injury, reduced ROS levels, increased MnSOD activities, mitigated mitochondrial dysfunction, ameliorated the defects in the nucleus morphology,
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865207
08AnimalAnimal study (in vivo)Mechanism
In mice with acute lung injury, NMN ameliorated nuclear morphology defects.
In plain wordsIn mice with lung injury, NMN reduced defects in nuclear structure.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseNuclear morphology defects
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Cell viability and death · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
Moreover, supplementation of NMN alleviated lung pathologic injury, reduced ROS levels, increased MnSOD activities, mitigated mitochondrial dysfunction, ameliorated the defects in the nucleus morphology,
1 context sentence(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865208
09AnimalAnimal study (in vivo)Mechanism
In mice with acute lung injury, NMN cytoprotection accompanied mitonuclear protein imbalance.
In plain wordsIn mice with lung injury, NMN protection accompanied mitonuclear protein imbalance.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseMitonuclear protein imbalance
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Mitochondrial function · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
and these cytoprotective effects were accompanied by preserving mitonuclear interaction (including mitonuclear protein imbalance and the mitochondrial unfolded protein response, UPR^mt).
2 context sentences(design, population, supporting numbers)
Summary · context
Taken together, our results indicated that NMN pretreatment ameliorated ALI by inducing mitonuclear protein imbalance and activating the UPR^mt in an SIRT1-dependent manner.
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865209
10AnimalAnimal study (in vivo)Mechanism
In mice with acute lung injury, NMN cytoprotection accompanied the mitochondrial unfolded protein response.
In plain wordsIn mice with lung injury, NMN protection accompanied the mitochondrial unfolded protein response.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseMitochondrial unfolded protein response
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Mitochondrial function · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
and these cytoprotective effects were accompanied by preserving mitonuclear interaction (including mitonuclear protein imbalance and the mitochondrial unfolded protein response, UPR^mt).
2 context sentences(design, population, supporting numbers)
Summary · context
Taken together, our results indicated that NMN pretreatment ameliorated ALI by inducing mitonuclear protein imbalance and activating the UPR^mt in an SIRT1-dependent manner.
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Report a problemFND-3553865210
11AnimalAnimal study (in vivo)Mechanism
In endotoxemic mice, SIRT1 probably regulated NAD+-mediated mitonuclear protein imbalance and the mitochondrial unfolded protein response during NMN pretreatment.
In plain wordsIn mice with endotoxemia, SIRT1 probably regulated mitochondrial and nuclear signaling during NMN pretreatment.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Direction not reportedSIRT1 regulation of mitonuclear signaling
Study
mousen: not reported in source
Endotoxin-induced acute lung injury in C57BL/6J mice
Outcome group
Receptor activity and mechanism · Respiratory
Studied dose
Dose not stated · 7 daysAs given in this study (mouse).
Source sentences
Summary
Furthermore, NAD⁺-mediated mitonuclear protein imbalance and UPR^mt are probably regulated by deacetylase Sirtuin1 (SIRT1).
2 context sentences(design, population, supporting numbers)
Summary · context
In the current study, C57BL/6J mice were administrated with lipopolysaccharide 15 mg/kg to induce endotoxin-induced ALI and investigated whether the NAD⁺ precursor nicotinamide mononucleotide (NMN) could preserve mitonuclear interaction and alleviate ALI.
Summary · context
After pretreatment with NMN for 7 days, NAD⁺ levels in the mitochondrial, nucleus, and total intracellular were significantly increased in endotoxemia mice.
Report a problemFND-3553865211

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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MeSH terms

Keywords

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