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Cited by 437Genetics, Aging, and Longevity in Model OrganismsNF-κB Signaling PathwaysExercise and Physiological Responses

The DOI matches its Crossref record; 119 of the 120 references it cites were found in a registry or an index.

The Molecular Inflammatory Process in Aging

Chung, Hae Young, Sung, Bokyung, Jung, Kyung Jin, Zou, Yani, Yu, Byung Pal·2006·Antioxidants & Redox Signaling
DOI 10.1089/ars.2006.8.572
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Abstract

Emerging pathological evidence indicates that major chronic aging-related diseases such as atherosclerosis, arthritis, dementia, osteoporosis, and cardiovascular diseases, are inflammation-related. In this review, inflammation is examined as a possible underlying basis for the molecular alterations that link aging and age-related pathological processes. A proposal for the molecular inflammation hypothesis of the aging views the redox derangement that occurs during aging as the major factor for increased risk for age-related inflammation. Accumulated data strongly indicate the activation of redox-sensitive transcription factors and dysregulated gene expression under the age-related oxidative stress seems to be the major culprits. Key players involved in the inflammatory process are the age-related upregulation of NF-kappaB, IL-1beta, IL-6, TNFalpha, cyclooxygenase-2, adhesion molecules, and inducible NO synthase. Furthermore, data are presented on the molecular events involved in age-related NF-kappaB activation and phosphorylation by IkappaB kinase/NIK and MAPKs. Experimental data on anti-aging calorie restriction (CR) for its antiinflammatory efficacy by suppressing the upregulated proinflammatory mediators will be reviewed. Also, the involvement of another super family of transcription factors, PPARs (PPARalpha, gamma) as regulators of proinflammatory responses and NF-kappaB signaling pathway is described as well as a discussion on the physiological significance of a well-maintained balance between NF-kappaB and PPARs.

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Crossref · 10.1089/ars.2006.8.572

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Research works printed but not linked: 6

  1. Bazan NG, 1989, Prog Clin Biol Res, 312, 15
  2. Bodamyali T, 2000, Birkhaüser Verlag, 11
  3. 10.1379/1466-1268(2004)009<0099:HSTPAA>2.0.CO;2 · DOI
  4. Kwon HJ, 2001, J Am Aging Assoc, 24, 161
  5. Maeda H, 1998, Biochemistry (Mosc), 63, 854
  6. Wahli W, 2002, Swiss Med Wkly, 132, 83

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Metadata

Authors
Chung, H. Y., Sung, B., Jung, K. J., Zou, Y., & Yu, B. P.
Affiliations
  • Pusan National University (KR)
  • The University of Texas at San Antonio Health Science Center (US)
ORCID
Venue
Antioxidants & Redox Signaling
Publisher
SAGE Publications
Published
2006-03
Volume
8
Issue
3-4
Pages
572-581
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
DOI
10.1089/ars.2006.8.572
OpenAlex
W2045601200
Cited by
437
References
120
Citations by year
2026: 6 · 2025: 18 · 2024: 10 · 2023: 19 · 2022: 17 · 2021: 25 · 2020: 26 · 2019: 13 · 2018: 21 · 2017: 17 · 2016: 21 · 2015: 21 · 2014: 27 · 2013: 22 · 2012: 20
FWCI
3.30
Type
journal article
Language
en
Open access
closed
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
Keywords
aging, inflammation, oxidative stress, redox imbalance, NF-κB signaling, IκB kinase, mitogen-activated protein kinase, peroxisome proliferator-activated receptors, caloric restriction, anti-aging, inflammatory cytokines, cyclooxygenase-2, inducible nitric oxide synthase, adhesion molecules, age-related diseases
MeSH terms
Aging, Animals, Humans, Inflammation, Models, Biological, Oxidation-Reduction, Up-Regulation, NF-kappa B, Caloric Restriction, Peroxisome Proliferator-Activated Receptors

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