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

The molecular inflammatory process in aging

Chung, Hae Young, Sung, Bokyung, Jung, Kyung Jin, Zou, Yani, Yu, Byung Pal·2006·Antioxidants & Redox Signaling

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.

Integrity signals

Registry

Crossref · 10.1089/ars.2006.8.572

Cites

119 of 119 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Flagged first, then by citations

1 of the 120 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

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)
Venue
Antioxidants & Redox Signaling
Published
2006-03
Volume
8
Issue
3-4
Pages
572-581
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
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 › Rehabilitation › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review