Nicotinamide Mononucleotide Alleviates the Development of Fibrotic Cataract by Modulating the Nrf2/FPN1 Signaling Pathway.

Bao X, Pan Y, Xu Y, Xing Y

FASEB journal : official publication of the Federation of American Societies for Experimental Biology1 Dec 2025

PMID41416389DOI10.1096/fj.202502783rrrPepBankPUB-41416389

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 study14

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

01AnimalAnimal study (in vivo)Efficacy outcome
In cataract mice, NMN restored lens architecture.
In plain wordsIn mice with cataracts, NMN restored lens structure.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Direction not reportedLens architecture
Study
mousen: not reported in source
ASC mouse model
Outcome group
Vision and retina · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vivo, NMN restores lens architecture, reduces fibrosis, and normalizes ferroptosis markers Fe²⁺, MDA reduction, and GSH restoration through Nrf2/FPN1 pathway activation.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, an ASC mouse model received NMN, followed by H&E, Masson, ferroptosis-related markers, and protein expression.
Report a problemFND-4141638910
02AnimalAnimal study (in vivo)Efficacy outcome
In cataract mice, NMN reduced lens fibrosis.
In plain wordsIn mice with cataracts, NMN reduced lens scarring.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLens fibrosis
Study
mousen: not reported in source
ASC mouse model
Outcome group
Vision and retina · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vivo, NMN restores lens architecture, reduces fibrosis, and normalizes ferroptosis markers Fe²⁺, MDA reduction, and GSH restoration through Nrf2/FPN1 pathway activation.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, an ASC mouse model received NMN, followed by H&E, Masson, ferroptosis-related markers, and protein expression.
Report a problemFND-4141638911
03AnimalAnimal study (in vivo)Mechanism
In cataract mice, NMN normalized Fe<sup>2+</sup> levels through Nrf2/FPN1 pathway activation.
In plain wordsIn mice with cataracts, NMN normalized iron levels through Nrf2/FPN1 signaling.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Direction not reportedLens Fe2+
Study
mousen: not reported in source
ASC mouse model
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vivo, NMN restores lens architecture, reduces fibrosis, and normalizes ferroptosis markers Fe²⁺, MDA reduction, and GSH restoration through Nrf2/FPN1 pathway activation.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, an ASC mouse model received NMN, followed by H&E, Masson, ferroptosis-related markers, and protein expression.
Report a problemFND-4141638912
04AnimalAnimal study (in vivo)Mechanism
In cataract mice, NMN reduced MDA through Nrf2/FPN1 pathway activation.
In plain wordsIn mice with cataracts, NMN reduced MDA through Nrf2/FPN1 signaling.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLens MDA
Study
mousen: not reported in source
ASC mouse model
Outcome group
Oxidative stress · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vivo, NMN restores lens architecture, reduces fibrosis, and normalizes ferroptosis markers Fe²⁺, MDA reduction, and GSH restoration through Nrf2/FPN1 pathway activation.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, an ASC mouse model received NMN, followed by H&E, Masson, ferroptosis-related markers, and protein expression.
Report a problemFND-4141638913
05AnimalAnimal study (in vivo)Mechanism
In cataract mice, NMN restored GSH through Nrf2/FPN1 pathway activation.
In plain wordsIn mice with cataracts, NMN restored GSH through Nrf2/FPN1 signaling.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseLens GSH
Study
mousen: not reported in source
ASC mouse model
Outcome group
Oxidative stress · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vivo, NMN restores lens architecture, reduces fibrosis, and normalizes ferroptosis markers Fe²⁺, MDA reduction, and GSH restoration through Nrf2/FPN1 pathway activation.
1 context sentence(design, population, supporting numbers)
Summary · context
In vivo, an ASC mouse model received NMN, followed by H&E, Masson, ferroptosis-related markers, and protein expression.
Report a problemFND-4141638914
06LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN inhibited TGF-β2-induced lipid ROS elevation.
In plain wordsIn cells, NMN reduced lipid reactive oxygen species induced by TGF-β2.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseLipid ROS
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Oxidative stress · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vitro, NMN inhibits TGF-β2-induced upregulation of ferroptosis markers lipid ROS, MDA, and Fe²⁺ and prevents GSH downregulation in SRA01/04 cells;
Report a problemFND-4141638901
07LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN inhibited TGF-β2-induced MDA elevation.
In plain wordsIn cells, NMN reduced MDA elevation induced by TGF-β2.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseMDA
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Oxidative stress · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vitro, NMN inhibits TGF-β2-induced upregulation of ferroptosis markers lipid ROS, MDA, and Fe²⁺ and prevents GSH downregulation in SRA01/04 cells;
Report a problemFND-4141638902
08LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN inhibited TGF-β2-induced Fe<sup>2+</sup> elevation.
In plain wordsIn cells, NMN reduced iron elevation induced by TGF-β2.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseFe2+
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vitro, NMN inhibits TGF-β2-induced upregulation of ferroptosis markers lipid ROS, MDA, and Fe²⁺ and prevents GSH downregulation in SRA01/04 cells;
Report a problemFND-4141638903
09LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN prevented TGF-β2-induced GSH downregulation.
In plain wordsIn cells, NMN prevented GSH reduction induced by TGF-β2.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseGSH
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Oxidative stress · Eye
Studied dose
Dose not stated
Source sentences
Summary
In vitro, NMN inhibits TGF-β2-induced upregulation of ferroptosis markers lipid ROS, MDA, and Fe²⁺ and prevents GSH downregulation in SRA01/04 cells;
Report a problemFND-4141638904
10LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN reversed E-cadherin downregulation.
In plain wordsIn cells, NMN restored reduced E-cadherin expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseE-cadherin
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
it reverses the EMT marker E-cadherin downregulation while suppressing collagen I, IV, and α-SMA expression.
Report a problemFND-4141638905
11LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN suppressed collagen I expression.
In plain wordsIn cells, NMN reduced collagen I expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseCollagen I
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
it reverses the EMT marker E-cadherin downregulation while suppressing collagen I, IV, and α-SMA expression.
Report a problemFND-4141638906
12LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN suppressed collagen IV expression.
In plain wordsIn cells, NMN reduced collagen IV expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseCollagen IV
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
it reverses the EMT marker E-cadherin downregulation while suppressing collagen I, IV, and α-SMA expression.
Report a problemFND-4141638907
13LabIn vitro (cells)Mechanism
In SRA01/04 cells, NMN suppressed α-SMA expression.
In plain wordsIn cells, NMN reduced α-SMA expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Decreaseα-SMA
Study
n: not reported in source
TGF-β2-treated SRA01/04 cells
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
it reverses the EMT marker E-cadherin downregulation while suppressing collagen I, IV, and α-SMA expression.
Report a problemFND-4141638908

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).

14LabNot a test of NMN (nicotinamide mononucleotide) aloneIn vitro (cells)Mechanism
In SRA01/04 cells, ML385 eliminated NMN protective effects, indicating Nrf2 dependence.
In plain wordsIn cells, ML385 removed NMN protection, which indicates dependence on Nrf2.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseNrf2-dependent protection
Study
n: not reported in source
SRA01/04 cells with Nrf2 inhibitor ML385
Outcome group
Receptor activity and mechanism · Eye
Source sentences
Summary
These protective effects are Nrf2-dependent, as ML385 deletes NMN's benefits.
1 context sentence(design, population, supporting numbers)
Summary · context
In vitro, TGF-β2-treated SRA01/04 cells were assessed for GSH, MDA, and Fe²⁺ levels, and the effects of NMN on cell viability, ROS levels, and GPX4, FTH1, Nrf2, and FPN1, ACSL4 protein expression were evaluated in SRA01/04 cells with/without NMN or Nrf2 inhibitor ML385.
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-4141638909

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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