Nicotinamide mononucleotide attenuates isoproterenol-induced cardiac fibrosis by regulating oxidative stress and Smad3 acetylation.

Wu K, Li B, Lin Q, Xu W, Zuo W, Li J, Liu N, Tu T, Zhang B, Xiao Y, Liu Q

Life sciences3 Mar 2021Cited by 45 (Europe PMC)

PMID33675899DOI10.1016/j.lfs.2021.119299PepBankPUB-33675899

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 study11

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice exposed to ISO, NMN alleviated cardiac dysfunction.
In plain wordsIn mice exposed to ISO, NMN reduced cardiac dysfunction compared with ISO alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseCardiac dysfunction
Study
mousen: not reported in source
Isoproterenol-induced cardiac fibrosis
Comparator
ISO without NMN
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated · intraperitoneal injectionAs given in this study (mouse).
Source sentences
Summary
ISO treatment induced cardiac dysfunction, fibrosis, and hypertrophy in vivo, whereas NMN alleviated these changes.
1 context sentence(design, population, supporting numbers)
Summary · context
Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by intraperitoneal injection.
Report a problemFND-3367589901
02AnimalAnimal study (in vivo)Efficacy outcome
In mice exposed to ISO, NMN alleviated cardiac fibrosis.
In plain wordsIn mice exposed to ISO, NMN reduced cardiac fibrosis compared with ISO alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseCardiac fibrosis
Study
mousen: not reported in source
Isoproterenol-induced cardiac fibrosis
Comparator
ISO without NMN
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated · intraperitoneal injectionAs given in this study (mouse).
Source sentences
Summary
ISO treatment induced cardiac dysfunction, fibrosis, and hypertrophy in vivo, whereas NMN alleviated these changes.
1 context sentence(design, population, supporting numbers)
Summary · context
Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by intraperitoneal injection.
Report a problemFND-3367589902
03AnimalAnimal study (in vivo)Efficacy outcome
In mice exposed to ISO, NMN alleviated cardiac hypertrophy.
In plain wordsIn mice exposed to ISO, NMN reduced heart enlargement compared with ISO alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseCardiac hypertrophy
Study
mousen: not reported in source
Isoproterenol-induced cardiac fibrosis
Comparator
ISO without NMN
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated · intraperitoneal injectionAs given in this study (mouse).
Source sentences
Summary
ISO treatment induced cardiac dysfunction, fibrosis, and hypertrophy in vivo, whereas NMN alleviated these changes.
1 context sentence(design, population, supporting numbers)
Summary · context
Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by intraperitoneal injection.
Report a problemFND-3367589903
04AnimalAnimal study (in vivo)Mechanism
In mice exposed to ISO, NMN restored the NAD+/SIRT1 axis.
In plain wordsIn mice exposed to ISO, NMN restored NAD+/SIRT1 signaling compared with ISO alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseNAD+/SIRT1 axis
Study
mousen: not reported in source
Isoproterenol-induced cardiac fibrosis
Comparator
ISO without NMN
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated · intraperitoneal injectionAs given in this study (mouse).
Source sentences
Summary
Mechanistically, NMN restored the NAD⁺/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β.
1 context sentence(design, population, supporting numbers)
Summary · context
Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by intraperitoneal injection.
Report a problemFND-3367589905
05AnimalAnimal study (in vivo)Mechanism
In mice exposed to ISO, NMN inhibited oxidative stress.
In plain wordsIn mice exposed to ISO, NMN reduced oxidative stress compared with ISO alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseOxidative stress
Study
mousen: not reported in source
Isoproterenol-induced cardiac fibrosis
Comparator
ISO without NMN
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated · intraperitoneal injectionAs given in this study (mouse).
Source sentences
Summary
Mechanistically, NMN restored the NAD⁺/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β.
1 context sentence(design, population, supporting numbers)
Summary · context
Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by intraperitoneal injection.
Report a problemFND-3367589906
06AnimalAnimal study (in vivo)Mechanism
In mice exposed to ISO, NMN inhibited Smad3 acetylation.
In plain wordsIn mice exposed to ISO, NMN reduced Smad3 acetylation compared with ISO alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSmad3 acetylation
Study
mousen: not reported in source
Isoproterenol-induced cardiac fibrosis
Comparator
ISO without NMN
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated · intraperitoneal injectionAs given in this study (mouse).
Source sentences
Summary
Mechanistically, NMN restored the NAD⁺/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β.
1 context sentence(design, population, supporting numbers)
Summary · context
Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by intraperitoneal injection.
Report a problemFND-3367589907
07LabIn vitro (cells)Efficacy outcome
In cardiac fibroblasts stimulated with TGF-β, NMN suppressed activation.
In plain wordsIn cells, NMN reduced cardiac fibroblast activation compared with TGF-β alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseFibroblast activation
Study
n: not reported in source
TGF-β-stimulated cardiac fibroblasts
Comparator
TGF-β without NMN
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Additionally, NMN suppressed CFs activation stimulated by TGF-β in vitro.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, cardiac fibroblasts (CFs) were stimulated by transforming growth factor-beta (TGF-β) with or without NMN and sirtinol, a SIRT1 inhibitor.
Report a problemFND-3367589904
08LabIn vitro (cells)Mechanism
In TGF-β-stimulated cardiac fibroblasts, NMN restored the NAD+/SIRT1 axis.
In plain wordsIn cells, NMN restored NAD+/SIRT1 signaling compared with TGF-β alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseNAD+/SIRT1 axis
Study
n: not reported in source
TGF-β-stimulated cardiac fibroblasts
Comparator
TGF-β without NMN
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Mechanistically, NMN restored the NAD⁺/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, cardiac fibroblasts (CFs) were stimulated by transforming growth factor-beta (TGF-β) with or without NMN and sirtinol, a SIRT1 inhibitor.
Report a problemFND-3367589908
09LabIn vitro (cells)Mechanism
In TGF-β-stimulated cardiac fibroblasts, NMN inhibited oxidative stress.
In plain wordsIn cells, NMN reduced oxidative stress compared with TGF-β alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseOxidative stress
Study
n: not reported in source
TGF-β-stimulated cardiac fibroblasts
Comparator
TGF-β without NMN
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Mechanistically, NMN restored the NAD⁺/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, cardiac fibroblasts (CFs) were stimulated by transforming growth factor-beta (TGF-β) with or without NMN and sirtinol, a SIRT1 inhibitor.
Report a problemFND-3367589909
10LabIn vitro (cells)Mechanism
In TGF-β-stimulated cardiac fibroblasts, NMN inhibited Smad3 acetylation.
In plain wordsIn cells, NMN reduced Smad3 acetylation compared with TGF-β alone.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSmad3 acetylation
Study
n: not reported in source
TGF-β-stimulated cardiac fibroblasts
Comparator
TGF-β without NMN
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Mechanistically, NMN restored the NAD⁺/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, cardiac fibroblasts (CFs) were stimulated by transforming growth factor-beta (TGF-β) with or without NMN and sirtinol, a SIRT1 inhibitor.
Report a problemFND-3367589910

Studies that did not test the peptide alone1

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).

11LabNot a test of NMN (nicotinamide mononucleotide) aloneIn vitro (cells)Mechanism
In cardiac fibroblasts, sirtinol partly antagonized NMN's protective effects.
In plain wordsIn cells, sirtinol reduced NMN's protective effects compared with NMN without sirtinol.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSirtinol antagonism
Study
n: not reported in source
TGF-β-stimulated cardiac fibroblasts
Comparator
NMN without sirtinol
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
However, the protective effects of NMN were partly antagonized by sirtinol in vitro.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, cardiac fibroblasts (CFs) were stimulated by transforming growth factor-beta (TGF-β) with or without NMN and sirtinol, a SIRT1 inhibitor.
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-3367589911

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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