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Cited by 305Genetics, Aging, and Longevity in Model OrganismsExercise and Physiological ResponsesNF-κB Signaling Pathways

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.

The Inflammation Hypothesis of Aging: Molecular Modulation by Calorie Restriction

Chung, Hae Young, Kim, Hyon Jeen, Kim, Jung Won, Yu, Byung Pal·2001·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2001.tb05662.x
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Abstract

A bstract: Current evidence strongly indicates that reactive oxygen species (ROS) and reactive nitrogen species (RNS) are widely implicated in the inflammatory process. However, mechanistic information is not readily available on the extent to which ROS/RNS contributes to the proinflammatory states of the aging process. The involvement of the underlying inflammation during the aging process and the molecular delineation of anti‐inflammatory action of calorie restriction (CR) is described. Age‐related upregulations of NF‐κB, IL‐β, IL‐6, TNFα, cyclooxygenase‐2, and inducible NO synthase are all attenuated by CR. The suppression of the NF‐κB activation was accomplished by blocking the dissociation of inhibitory IκBα and IκBβ by CR. These findings provide underlying molecular insights into the anti‐inflammatory action of CR in relation to the aging process. Based on these and other available data, it is suggested that the “Inflammation Hypothesis of Aging” supports the molecular basis of the inflammatory process as a plausible cause of the aging process.

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Crossref · 10.1111/j.1749-6632.2001.tb05662.x

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36 of 36 references verified0 citation errors · 0 not checkable

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  • Caloric restriction affects NF-κB, mTOR, AMPK, and MAPK pathways involved in ageing and inflammation, downregulating inflammatory markers such as IL-6 and IL-1β.

    “NF-κB, mTOR, AMPK, and MAPK are pathways that are involved in both ageing and inflammation and have been shown to be affected by caloric restriction, resulting in downregulation of inflammatory markers, such as IL-6 and IL-1β191,192.”

    From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [192]

  • NF-κB, mTOR, and MAPK pathways closely related to aging and inflammation are modulated by caloric restriction that downregulates the activation of IL-1β, IL-6, and TNF-α genes, hence the pro-inflammatory state.

    “NF-κB, mechanistic target of rapamycin (mTOR), and MAPK, pathways closely related to aging and inflammation are modulated by caloric restriction that downregulates the activation of IL-1β, IL-6, and tumor necrosis factor (TNF)-α genes, hence the pro-inflammatory state (20, 91, 92).”

    From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [92]

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Research works printed but not linked: 6

  1. Muray R.K. et al.1993. Lipids of physiologic significance.InHarper's Biochemistry. Appleton and Lange Eds.:143. Prentice Hall. London.
  2. Kim J.W. 1998. Attenuation of free radical generation related to cardiac arachidonate cascade by dietary restriction during aging. M.S. Thesis Pusan National Univ. Pusan Korea.
  3. Kim H.J. 1999. Regulation of inflammatory enzymes via NF‐κB in the aging process. M.S. Thesis Pusan National Univ. Pusan Korea.
  4. Kim Y.J. Antiaging mechanism of fish oil. M.S. Thesis Pusan National Univ. Pusan Korea.
  5. Roitt I.M. J. Brostoff & D.K. Male. 1993. The cytokine network.InImmunology: 8‐15. Mosby. St. Louis.
  6. Kwon H.J. 2000. Gene expression of proinflammatory proteins and NF‐κB activation in the aging process. M.S. Thesis Pusan National Univ. Pusan Korea.

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Metadata

Authors
Chung, H. Y., Kim, H. J., Kim, J. W., & Yu, B. P.
Affiliations
Pusan National University (KR)
Corresponding author
Chung, Hae Young
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2001-04
Volume
928
Issue
1
Pages
327-335
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2001.tb05662.x
OpenAlex
W2163849426
Cited by
305
References
36
Citations by year
2026: 2 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 13 · 2020: 12 · 2019: 10 · 2018: 11 · 2017: 8 · 2016: 11 · 2015: 12 · 2014: 11 · 2013: 19 · 2012: 10
FWCI
4.43
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1760 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
caloric restriction, reactive oxygen species, reactive nitrogen species, NF-κB, IκBα, IκBβ, inflammatory cytokines, cyclooxygenase-2, inducible nitric oxide synthase, aging
MeSH terms
NF-KappaB Inhibitor alpha, Aging, Animals, Energy Intake, DNA-Binding Proteins, Food Deprivation, Inflammation, Isoenzymes, Mitochondria, Models, Biological, Nitric Oxide, Prostaglandin-Endoperoxide Synthases, Prostaglandins, Superoxide Dismutase, Tumor Necrosis Factor-alpha, Interleukin-6, NF-kappa B, Reactive Oxygen Species, Mice, Knockout, Oxidative Stress, Nitric Oxide Synthase, I-kappa B Proteins, Mice, Cyclooxygenase 2, Nitric Oxide Synthase Type II

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