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

Sonya Vasto; Giuseppina Candore; Giuseppina Colonna Romano; Calogero Caruso; Domenico Lio; Claudia Maria Rizzo; 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

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

Risultato della ricerca: Article

114 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

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All Science Journal Classification (ASJC) codes

Medicine(all)
Pharmacology
Drug Discovery

Cita questo

Vasto, S., Candore, G., Colonna Romano, G., Caruso, C., Lio, D., Rizzo, C. M., Nuzzo, D., Cevenini, Scurti, Palmas, Pini, Franceschi, C., Duro, G., & Capri, M. (2010). Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches. CURRENT PHARMACEUTICAL DESIGN, 16, 609-618.

Age-Related Inflammation: the Contribution of Different Organs, Tissues andSystems. How to Face it for Therapeutic Approaches. / Vasto, Sonya ; Candore, Giuseppina ; Colonna Romano, Giuseppina ; Caruso, Calogero ; Lio, Domenico ; Rizzo, Claudia Maria; 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

Vasto, Sonya ; Candore, Giuseppina ; Colonna Romano, Giuseppina ; Caruso, Calogero ; Lio, Domenico ; Rizzo, Claudia Maria ; 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.

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

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AU - Vasto, Sonya

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AU - Colonna Romano, Giuseppina

AU - Caruso, Calogero

AU - Lio, Domenico

AU - Rizzo, Claudia Maria

AU - Nuzzo, Domenico

AU - Cevenini, null

AU - Scurti, null

AU - Palmas, null

AU - Pini, null

AU - Franceschi, Claudio

AU - Duro, Giovanni

AU - Capri, Miriam

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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

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JO - CURRENT PHARMACEUTICAL DESIGN

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