Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches

Calogero Caruso; Giuseppina Colonna Romano; Giuseppina Candore; Claudia Maria Rizzo; Domenico Lio; Sonya Vasto; Domenico Nuzzo; null Cevenini; null Scurti; null Palmas; null Pini; Claudio Franceschi; Giovanni Duro; Miriam Capri

Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches

Calogero Caruso, Giuseppina Colonna Romano, Giuseppina Candore, Claudia Maria Rizzo, Domenico Lio, Sonya Vasto, Domenico Nuzzo, Cevenini, Scurti, Palmas, Pini, Claudio Franceschi, Giovanni Duro, Miriam Capri

Risultato della ricerca: Article › peer review

128 Citazioni (Scopus)

Abstract

A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of proinflammatorycytokines and inflammatory markers (“inflamm-ageing”). This status may slowly damage one or several organs, especiallywhen unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together withthe onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immunesystem and ecosystems (gut microbiota) to age-related inflammation (“inflamm-ageing”) will be discussed in this review in the context ofits onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteractthe different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented

Lingua originale	English
pagine (da-a)	609-618
Numero di pagine	10
Rivista	CURRENT PHARMACEUTICAL DESIGN
Volume	16
Stato di pubblicazione	Published - 2010

All Science Journal Classification (ASJC) codes

Medicine(all)
Pharmacology
Drug Discovery

Accesso al documento

OA Link

Fingerprint Entra nei temi di ricerca di 'Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches'. Insieme formano una fingerprint unica.

Cita questo

Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches. / Caruso, Calogero ; Colonna Romano, Giuseppina ; Candore, Giuseppina ; Rizzo, Claudia Maria ; Lio, Domenico ; Vasto, Sonya; Nuzzo, Domenico; Cevenini; Scurti; Palmas; Pini; Franceschi, Claudio; Duro, Giovanni; Capri, Miriam.

In: CURRENT PHARMACEUTICAL DESIGN, Vol. 16, 2010, pag. 609-618.

Risultato della ricerca: Article › peer review

Caruso, Calogero ; Colonna Romano, Giuseppina ; Candore, Giuseppina ; Rizzo, Claudia Maria ; Lio, Domenico ; Vasto, Sonya ; Nuzzo, Domenico ; Cevenini ; Scurti ; Palmas ; Pini ; Franceschi, Claudio ; Duro, Giovanni ; Capri, Miriam. / Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches. In: CURRENT PHARMACEUTICAL DESIGN. 2010 ; Vol. 16. pagg. 609-618.

@article{0c44f56a871a4579a19b8cb16b8afead,

title = "Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches",

abstract = "A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of proinflammatorycytokines and inflammatory markers (“inflamm-ageing”). This status may slowly damage one or several organs, especiallywhen unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together withthe onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immunesystem and ecosystems (gut microbiota) to age-related inflammation (“inflamm-ageing”) will be discussed in this review in the context ofits onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteractthe different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented",

author = "Calogero Caruso and {Colonna Romano}, Giuseppina and Giuseppina Candore and Rizzo, {Claudia Maria} and Domenico Lio and Sonya Vasto and Domenico Nuzzo and Cevenini and Scurti and Palmas and Pini and Claudio Franceschi and Giovanni Duro and Miriam Capri",

year = "2010",

language = "English",

volume = "16",

pages = "609--618",

journal = "CURRENT PHARMACEUTICAL DESIGN",

issn = "1381-6128",

}

TY - JOUR

T1 - Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches

AU - Caruso, Calogero

AU - Colonna Romano, Giuseppina

AU - Candore, Giuseppina

AU - Rizzo, Claudia Maria

AU - Lio, Domenico

AU - Vasto, Sonya

AU - Nuzzo, Domenico

AU - Cevenini, null

AU - Scurti, null

AU - Palmas, null

AU - Pini, null

AU - Franceschi, Claudio

AU - Duro, Giovanni

AU - Capri, Miriam

PY - 2010

Y1 - 2010

N2 - A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of proinflammatorycytokines and inflammatory markers (“inflamm-ageing”). This status may slowly damage one or several organs, especiallywhen unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together withthe onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immunesystem and ecosystems (gut microbiota) to age-related inflammation (“inflamm-ageing”) will be discussed in this review in the context ofits onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteractthe different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented

AB - A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of proinflammatorycytokines and inflammatory markers (“inflamm-ageing”). This status may slowly damage one or several organs, especiallywhen unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together withthe onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immunesystem and ecosystems (gut microbiota) to age-related inflammation (“inflamm-ageing”) will be discussed in this review in the context ofits onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteractthe different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented

UR - http://hdl.handle.net/10447/77294

M3 - Article

VL - 16

SP - 609

EP - 618

JO - CURRENT PHARMACEUTICAL DESIGN

JF - CURRENT PHARMACEUTICAL DESIGN

SN - 1381-6128

ER -