Cited by 686Interstitial Lung Diseases and Idiopathic Pulmonary FibrosisRedox biology and oxidative stressGenomics, phytochemicals, and oxidative stress

Reversal of persistent fibrosis in aging by targeting Nox4-Nrf2 redox imbalance

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Hecker, Louise, Logsdon, Naomi J., Kurundkar, Deepali, Kurundkar, Ashish, Bernard, Karen, Hock, Thomas, Meldrum, Eric, Sanders, Yan Y. +1 more·2014·Science Translational Medicine

Abstract

Fibrosis resolution is impaired by aging and is mediated by altered cellular redox homeostasis because of a Nox4-Nrf2 imbalance that promotes an apoptosis-resistant myofibroblast phenotype.

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Crossref · 10.1126/scitranslmed.3008182

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  • Bleomycin lung injury induces a molecular signature of senescence, and age-dependent accumulation of senescent myofibroblasts may impede fibrosis resolution following bleomycin exposure.

    “Bleomycin lung injury induces a molecular signature of senescence1617 and age-dependent accumulation of senescent myofibroblasts may impede fibrosis resolution following bleomycin exposure3.”

    From Cellular senescence mediates fibrotic pulmonary disease (2017) · cites this paper as [3]

  • Impaired capacity to resolve fibrotic bleomycin injury has been associated with accumulation of apoptosis-resistant, senescent myofibroblasts.

    “Critically, impaired capacity to resolve fibrotic bleomycin injury has been associated with accumulation of apoptosis-resistant, senescent myofibroblasts3.”

    From Cellular senescence mediates fibrotic pulmonary disease (2017) · cites this paper as [3]

  • Cellular senescence has been linked to the pathogenesis of chronic lung diseases such as COPD or IPF.

    “cellular senescence has been linked to the pathogenesis of chronic lung diseases such as chronic obstructive pulmonary disease [14, 15] or IPF [16–20].”

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Authors
Hecker, L., Logsdon, N. J., Kurundkar, D., Kurundkar, A., Bernard, K., Hock, T., Meldrum, E., Sanders, Y. Y., & Thannickal, V. J.
Affiliations
  • University of Alabama at Birmingham (US)
  • Genkyotex (Switzerland) (CH)
Corresponding author
  • Hecker, Louise
  • Thannickal, Victor J.
Venue
Science Translational Medicine
Published
2014-04-09
Volume
6
Issue
231
Pages
231ra47-231ra47
ISSN
  • 1946-6234 (ISSN-L)
  • 1946-6242
OpenAlex
W2056269088
Cited by
686
References
48
Citations by year
2026: 32 · 2025: 51 · 2024: 57 · 2023: 69 · 2022: 53 · 2021: 70 · 2020: 70 · 2019: 58 · 2018: 53 · 2017: 58 · 2016: 53 · 2015: 36 · 2014: 24 · 2013: 1
FWCI
45.74
Type
journal article
Language
en
Open access
Locations
  • Science Translational Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • U.S. Department of Veterans Affairs (IK2 BX001477)
  • National Heart, Lung, and Blood Institute (R01HL094230, P50HL107181, P01HL114470)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR048311)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
Keywords
aging, NOX4, Nrf2, redox homeostasis, idiopathic pulmonary fibrosis, myofibroblasts, cellular senescence, apoptosis resistance, reactive oxygen species, NADPH oxidase, fibrosis resolution
MeSH terms
NADPH Oxidase 4, Aging, Animals, Antioxidants, Female, Fibroblasts, Humans, Mice, Inbred C57BL, Models, Biological, Oxidation-Reduction, Phenotype, Apoptosis, Oxidative Stress, NADPH Oxidases, NF-E2-Related Factor 2, Idiopathic Pulmonary Fibrosis, Lung Injury, Molecular Targeted Therapy

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