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Study · In vitro (cells) · 2025

4 results

SIRT1 Prevents Lens Epithelial Cell Senescence During Age-Related Cataract via Regulating p66Shc.

Liu H, Sun L, Mi Y, Gao Y, Luo J, Kang F, Bai Y, Yu X, Ge H

Aging cell26 Jun 2025Cited by 5 (Europe PMC)

PMID40569566 (opens in a new tab)PMCIDPMC12419841 (opens in a new tab)DOI10.1111/acel.70155 (opens in a new tab)PepBankPUB-40569566
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Summary

Lens epithelial cell (LEC) senescence is one of the key pathological processes of age-related cataract (ARC) and is associated with oxidative stress, mitochondrial dysfunction, and protein aggregation. This study aimed to elucidate the pathogenesis of LEC senescence in ARC. The protein expression level of silencing regulatory protein 1 (SIRT1) and aptamer protein (p66Shc) was quantified. Reactive oxygen species (ROS) and mitochondrial superoxide levels were measured to evaluate cellular oxidative stress. Senescence-associated protein expression (p21 and p53) and SA-β-galactosidase staining were employed to assess the aging status of LEC. Targeted metabolic analysis was conducted to explore energy changes during LEC senescence, and mitochondrial morphology and function were assessed in the cell models. The aging and damage conditions of the lens in ARC rats were evaluated through histological staining, transmission electron microscopy, expression of senescence-related proteins, and oxidative stress markers. We comprehensively investigated the downregulation of SIRT1 expression and the upregulation of p66Shc expression in human cataract samples, UVB-induced rat cataract models, and UVB-treated LEC. SIRT1 could alleviate UVB-induced oxidative stress, as well as mitochondrial dysfunction, inhibiting p66Shc expression in LEC. Nicotinamide mononucleotide (NMN) effectively alleviated the abnormal expression of aging-related proteins and inhibited mitochondrial morphological and functional disorders by activating SIRT1. In conclusion, NMN activated SIRT1, inhibiting mitochondrial dysfunction, oxidative stress, and senescence in LEC, delaying lens opacity. This mechanism could be associated with the onset and progression of ARC, providing a new strategy for its prevention and treatment.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01LabIn vitro (cells)Mechanism

    In lens epithelial cells, NMN alleviated abnormal aging-related protein expression through SIRT1 activation.

    In plain wordsIn cells from the lens, NMN reduced abnormal aging-related protein expression through SIRT1 activation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableAbnormal aging-related protein expression
    Study

    n: not reported in source

    lens epithelial cells
    Outcome group
    Aging markers · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Nicotinamide mononucleotide (NMN) effectively alleviated the abnormal expression of aging-related proteins and inhibited mitochondrial morphological and functional disorders by activating SIRT1.
    1 context sentence
    Summary · context
    Targeted metabolic analysis was conducted to explore energy changes during LEC senescence, and mitochondrial morphology and function were assessed in the cell models.
  2. 02LabIn vitro (cells)Mechanism

    In lens epithelial cells, NMN inhibited mitochondrial morphological disorders through SIRT1 activation.

    In plain wordsIn cells from the lens, NMN reduced abnormal mitochondrial structure through SIRT1 activation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMitochondrial morphological disorders
    Study

    n: not reported in source

    lens epithelial cells
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Nicotinamide mononucleotide (NMN) effectively alleviated the abnormal expression of aging-related proteins and inhibited mitochondrial morphological and functional disorders by activating SIRT1.
    1 context sentence
    Summary · context
    Targeted metabolic analysis was conducted to explore energy changes during LEC senescence, and mitochondrial morphology and function were assessed in the cell models.
  3. 03LabIn vitro (cells)Mechanism

    In lens epithelial cells, NMN inhibited mitochondrial functional disorders through SIRT1 activation.

    In plain wordsIn cells from the lens, NMN reduced mitochondrial dysfunction through SIRT1 activation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMitochondrial functional disorders
    Study

    n: not reported in source

    lens epithelial cells
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Nicotinamide mononucleotide (NMN) effectively alleviated the abnormal expression of aging-related proteins and inhibited mitochondrial morphological and functional disorders by activating SIRT1.
    1 context sentence
    Summary · context
    Targeted metabolic analysis was conducted to explore energy changes during LEC senescence, and mitochondrial morphology and function were assessed in the cell models.
  4. 04LabIn vitro (cells)Mechanism

    In lens epithelial cells, NMN activated SIRT1.

    In plain wordsIn cells from the lens, NMN activated SIRT1.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseSIRT1 activation
    Study

    n: not reported in source

    lens epithelial cells
    Outcome group
    Receptor activity and mechanism · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Nicotinamide mononucleotide (NMN) effectively alleviated the abnormal expression of aging-related proteins and inhibited mitochondrial morphological and functional disorders by activating SIRT1.
    1 context sentence
    Summary · context
    Targeted metabolic analysis was conducted to explore energy changes during LEC senescence, and mitochondrial morphology and function were assessed in the cell models.

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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