Cited by 1,203Genetics, Aging, and Longevity in Model OrganismsExercise and Physiological ResponsesAdvanced Glycation End Products research

Molecular inflammation: Underpinnings of aging and age-related diseases

Open access
Chung, Hae Young, Cesari, Matteo, Anton, Stephen, Marzetti, Emanuele, Giovannini, Silvia, Seo, Arnold Young, Carter, Christy, Yu, Byung Pal +1 more·2009·Ageing Research Reviews

Abstract

Recent scientific studies have advanced the notion of chronic inflammation as a major risk factor underlying aging and age-related diseases. In this review, low-grade, unresolved, molecular inflammation is described as an underlying mechanism of aging and age-related diseases, which may serve as a bridge between normal aging and age-related pathological processes. Accumulated data strongly suggest that continuous (chronic) upregulation of pro-inflammatory mediators (e.g., TNF-alpha, IL-1beta, IL-6, COX-2, iNOS) are induced during the aging process due to an age-related redox imbalance that activates many pro-inflammatory signaling pathways, including the NF-kappaB signaling pathway. These pro-inflammatory molecular events are discussed in relation to their role as basic mechanisms underlying aging and age-related diseases. Further, the anti-inflammatory actions of aging-retarding caloric restriction and exercise are reviewed. Thus, the purpose of this review is to describe the molecular roles of age-related physiological functional declines and the accompanying chronic diseases associated with aging. This new view on the role of molecular inflammation as a mechanism of aging and age-related pathogenesis can provide insights into potential interventions that may affect the aging process and reduce age-related diseases, thereby promoting healthy longevity.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.arr.2008.07.002

Cites

224 of 224 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Chronic inflammation is a cause or an important contributor to virtually every major age-related disease, both degenerative and hyperplastic.

    “Chronic inflammation, of course, is a cause of—or an important contributor to—virtually every major age-related disease, both degenerative and hyperplastic (109–111).”

    From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [109]

    The Introduction calls chronic inflammation a major underlying condition of many age-related diseases, including degenerative conditions and cancer. The Conclusion likewise describes it as a primary factor underlying numerous age-related diseases. Neither passage supports the stronger claim that it contributes to virtually every major age-related disease. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Low-level, chronic, sterile inflammation is a hallmark of aging that initiates or promotes most, if not all, major age-related diseases.

    “Low-level, chronic, “sterile” inflammation is a hallmark of aging that initiates or promotes most, if not all, major age-related diseases (Franceschi et al., 2007; Chung et al., 2009).”

    From Four faces of cellular senescence (2011) · cites this paper as Chung et al., 2009

    The Introduction describes chronic, low-grade inflammation as a possible link between aging and the pathogenesis of many age-related diseases; the Conclusion calls it a primary factor underlying aging and numerous age-related diseases. The copy does not characterize the inflammation as “sterile,” and its references to many or numerous diseases do not substantiate “most, if not all.” Page numbers were not available in the indexed passages. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Most age-related pathologies stem from low level chronic inflammation referred to as inflammaging or sterile inflammation, which can also result in premature aging.

    “most of the age-related pathologies stem from low level chronic inflammation referred to as inflammaging or sterile inflammation which can also result in premature aging (Franceschi et al., 2007; Chung et al., 2009; Franceschi and Campisi, 2014; Jurk et al., 2014).”
  • NF-κB regulates the expression of myokines such as TNF-α and IL-6, inducing chronic low-grade inflammation and apoptosis, increasing catabolic pathway activity and decreasing anabolic pathway activity in skeletal muscle, promoting loss of muscle mass and strength.

    “NF-κB regulates the expression of myokines such as TNF-α and IL-6, inducing chronic low-grade inflammation and apoptosis. These conditions increase catabolic pathway activity and decrease anabolic pathway activity in skeletal muscle, promoting the loss of muscle mass and strength [76, 114].”

    From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [114]

  • Persistent inflammation contributes to the development of several diseases, such as insulin resistance, dementia, rheumatoid arthritis, atherosclerosis, and cancer.

    “Chronic inflammation is an underlying cause of several pathological disorders including insulin resistance, dementia, rheumatoid arthritis, atherosclerosis, and cancer [1, 2].”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Chung HY Cheng KQ Chung GJ 2004 Molecular inflammation in aging process Nippon Ronen Igakkai Zasshi 41 357 364 15387272

Cited by

Sorted by citations

Authors
Chung, H. Y., Cesari, M., Anton, S., Marzetti, E., Giovannini, S., Seo, A. Y., Carter, C., Yu, B. P., & Leeuwenburgh, C.
Affiliations
  • University of Florida (US)
  • The University of Texas at San Antonio Health Science Center (US)
Corresponding author
  • Chung, Hae Young
  • Leeuwenburgh, Christiaan
Venue
Ageing Research Reviews
Publisher
Elsevier BV
Published
2009-01
Volume
8
Issue
1
Pages
18-30
ISSN
1568-1637 (ISSN-L)
OpenAlex
W2005822229
Cited by
1,203
References
224
Citations by year
2026: 34 · 2025: 41 · 2024: 71 · 2023: 66 · 2022: 70 · 2021: 87 · 2020: 98 · 2019: 80 · 2018: 75 · 2017: 76 · 2016: 86 · 2015: 85 · 2014: 62 · 2013: 76 · 2012: 59
FWCI
3.84
Type
journal article
Language
en
Open access
Locations
  • Ageing Research Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Heart Association
  • University of Florida
  • Pusan National University
  • National Institutes of Health
  • National Institute on Aging (AG17994, R01AG017994, AG-21042, R01AG021042, P30AG028740)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Keywords
chronic inflammation, aging, age-related diseases, pro-inflammatory mediators, TNF-α, IL-1β, interleukin-6, cyclooxygenase-2, inducible nitric oxide synthase, redox imbalance, NF-κB signaling, caloric restriction, physical activity, healthy longevity
MeSH terms
Aging, Animals, Disease, Humans, Inflammation, Models, Biological, Oxidation-Reduction, Oxidative Stress, Inflammation Mediators, MAP Kinase Signaling System

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