Inflamm‐aging: An Evolutionary Perspective on Immunosenescence

By Claudio Franceschi, M. Bonafè, S. Valensin, F. Olivieri, M. De Luca, E. Ottaviani, G. de Benedictis. 2000

4,917 citations recorded by the source corpus.

Subfields: Aging, Biological Psychiatry, Endocrine and Autonomic Systems

View Paper: https://www.semanticscholar.org/paper/9d98ff3b1db0079665146cf0c405598592055eb3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. M. Demaria
2. Steve Horvath
3. Luigi Ferrucci
4. P. Desprez
5. Adam Freund
6. Antero Salminen
7. J. Campisi
8. M. Levine

In Biological Psychiatry

1. J. Cryan
2. Ted G. Dinan
3. G. Clarke
4. C. Stanton
5. Andrew H. Miller
6. R. Stilling
7. L. Capuron
8. J. Kiecolt-Glaser

In Endocrine and Autonomic Systems

1. J. Campisi
2. M. Levine
3. Michael R. Irwin
4. F. Dhabhar
5. Esther M. Sternberg
6. Chandan K. Sen

Citations in the corpus

• NLRP3 inflammasome and its inhibitors: a review (2015, background): “…protect against disease and death, inappropriate activation of the NLRP3 inflammasome can contribute to the onset and progression of various diseases, particularly age-related diseases such as metabolic disorders and metabolic syndrome (Franceschi et al., 2000; Goldberg and Dixit, 2015).”
• Inflammatory Networks during Cellular Senescence: Causes and Consequences (2010, background): “Immunosenescence is caused primarily by an exhaustion of the pool of naïve T cells, clonal expansion among T and B cells, and the consequent shrinkage of “immunological space”; together, these phenomena reduce the body’s ability to respond to new antigens [12, 13].”
• Inflammation and its role in age-related macular degeneration (2016, background): “level inflammation has been linked with the development of various chronic conditions, such as cancer, diabetes, autoimmune diseases, as well as several obesity-related and neurodegenerative diseases [3, 4].”
• Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. (2004, background): “Indeed, it has been argued that a major characteristic of aging is a global reduction in the capacity to cope with a variety of stressors and a concomitant increase in proinflammatory status (110).”
• The neuropharmacology of butyrate: The bread and butter of the microbiota-gut-brain axis? (2016, background): “, 2010), especially in the light of the chronic inflammatory state known as inflamm-ageing (Franceschi et al., 2000) to which many tissues succumb, including the brain (Prenderville et al.”
• The Gut Microbiota and Alzheimer’s Disease (2017, neutral): “Aging is associated with an overstimulation of both innate and adaptive immune systems, resulting in a low-grade, chronic state of inflammation defined as inflammaging (for review, see [86, 87]), which may increase gut permeability (“leaky gut”) and bacterial translocation (for review, see [88, 89]).”
• Composition, variability, and temporal stability of the intestinal microbiota of the elderly (2010, background): “The aging intestine is subject to a number of physiological changes that impact on food digestion and absorption (25, 26) and immune function (27).”
• ESPEN guidelines on definitions and terminology of clinical nutrition. (2017, background): “Advanced ageing per se may contribute to the state of inflammation [13].”
• Age-Associated Microbial Dysbiosis Promotes Intestinal Permeability, Systemic Inflammation, and Macrophage Dysfunction (2017, neutral): “It has been theorized that gradual, cumulative, sub-clinical tissue damage occurs, which increases the burden of tissue repair and results in increasing background levels of pro-inflammatory cytokine production (Franceschi et al., 2000); however, the experimental evidence that would definitively pro”