CoChat
Sign Up
Cited by 454Genetics, Aging, and Longevity in Model OrganismsImmune Response and InflammationInflammasome and immune disorders

The DOI matches its Crossref record; 156 of the 159 references it cites were found in a registry or an index.

Innate immunity and inflammation in ageing: a key for understanding age-related diseases

Open access
Licastro, Federico, Candore, Giuseppina, Lio, Domenico, Porcellini, Elisa, Colonna-Romano, Giuseppina, Franceschi, Claudio, Caruso, Calogero·2005·Immunity & Ageing
DOI 10.1186/1742-4933-2-8PMC PMC1166571
Open this paper in CoChat — free accountOpen PDF

Abstract

The process of maintaining life for the individual is a constant struggle to preserve his/her integrity. This can come at a price when immunity is involved, namely systemic inflammation. Inflammation is not per se a negative phenomenon: it is the response of the immune system to the invasion of viruses or bacteria and other pathogens. During evolution the human organism was set to live 40 or 50 years; today, however, the immune system must remain active for much a longer time. This very long activity leads to a chronic inflammation that slowly but inexorably damages one or several organs: this is a typical phenomenon linked to ageing and it is considered the major risk factor for age-related chronic diseases. Alzheimer's disease, atherosclerosis, diabetes and even sarcopenia and cancer, just to mention a few - have an important inflammatory component, though disease progression seems also dependent on the genetic background of individuals. Emerging evidence suggests that pro-inflammatory genotypes are related to unsuccessful ageing, and, reciprocally, controlling inflammatory status may allow a better chance of successful ageing. In other words, age-related diseases are "the price we pay" for a life-long active immune system: this system has also the potential to harm us later, as its fine tuning becomes compromised. Our immune system has evolved to control pathogens, so pro-inflammatory responses are likely to be evolutionarily programmed to resist fatal infections with pathogens aggressively. Thus, inflammatory genotypes are an important and necessary part of the normal host responses to pathogens in early life, but the overproduction of inflammatory molecules might also cause immune-related inflammatory diseases and eventually death later. Therefore, low responder genotypes involved in regulation of innate defence mechanisms, might better control inflammatory responses and age-related disease development, resulting in an increased chance of long life survival in a "permissive" environment with reduced pathogen load, medical care and increased quality of life.

Overview

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 · 10.1186/1742-4933-2-8

Cites

156 of 156 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Schematic representation of inflammatory mechanisms involved in pathogenesis of atherosclerosis and plaque formation. Monocytes and macrophages are the protagonists of atherosclerotic processes.
Figure 1 Schematic representation of inflammatory mechanisms involved in pathogenesis of atherosclerosis and plaque formation. Monocytes and macrophages are the protagonists of atherosclerotic processes.CC BY · PubMed Central
Figure 2 Alzheimer's disease: amyloid deposition is one the main pathogenetic mechanism. Accumulation of Aβ peptide may be caused by 1) gene mutations (PS1, PS2 and APP human mutations in familial Alzheimer's disease) 2) genotype (and/or phenotype) favoring unbalanced inflammatory responses (pro-inflammatory genotype/anti-inflammatory genotype).
Figure 2 Alzheimer's disease: amyloid deposition is one the main pathogenetic mechanism. Accumulation of Aβ peptide may be caused by 1) gene mutations (PS1, PS2 and APP human mutations in familial Alzheimer's disease) 2) genotype (and/or phenotype) favoring unbalanced inflammatory responses (pro-inflammatory genotype/anti-inflammatory genotype).CC BY · PubMed Central

Verification

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?

Self-check

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

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

Citations

Cites

Show all 159 references

Research works printed but not linked: 2

  1. Mitchell RN, Cotran RS: Acute and Chronic Inflammation. Robbins Basic Pathology. 2003, Saunderrs, Philadelphia, USA
  2. Rudin E, Barzilai N: Inflammatory peptides derived from adipose tissue. Immun Ageing. 2005, 2: 1-10.1186/1742-4933-2-1. · DOI

Cited by

Sorted by citations

Items 301–400 of 454

Related

See all

Metadata

Authors
Licastro, F., Candore, G., Lio, D., Porcellini, E., Colonna-Romano, G., Franceschi, C., & Caruso, C.
Affiliations
  • University of Bologna (IT)
  • University of Palermo (IT)
  • Istituto Nazionale di Riposo e Cura per Anziani (IT)
Corresponding author
Licastro, Federico
ORCID
Venue
Immunity & Ageing
Publisher
Springer Science and Business Media LLC
Published
2005-05-18
Volume
2
Issue
1
Pages
8-8
ISSN
1742-4933 (ISSN-L)
DOI
10.1186/1742-4933-2-8
PMC
PMC1166571
OpenAlex
W2115145729
Cited by
453
References
159
Citations by year
2026: 2 · 2025: 9 · 2024: 13 · 2023: 9 · 2022: 15 · 2021: 33 · 2020: 24 · 2019: 34 · 2018: 23 · 2017: 30 · 2016: 23 · 2015: 24 · 2014: 33 · 2013: 24 · 2012: 29
FWCI
6.71
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Immunity & Ageing (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Nova Science Publishers (Nova Science Publishers, Inc.) (submittedVersion)
Funders
Ministero dell’Istruzione, dell’Università e della Ricerca
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
innate immunity, systemic inflammation, aging, age-related diseases, chronic inflammation, successful aging, evolutionary programming, Alzheimer's disease, atherosclerosis, diabetes mellitus, sarcopenia, cancer, immunosenescence

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