Abstract
Aging is a complex phenomenon driven by a variety of molecular alterations. A relevant feature of aging is chronic low-grade inflammation, termed "inflammaging." In type 2 diabetes mellitus (T2DM), many elements of aging appear earlier or are overrepresented, including consistent inflammaging. T2DM patients have an increased death rate, associated with an incremented inflammatory score. The source of this inflammation is debated. Recently, the senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammaging in both aging and T2DM. Different pathogenic mechanisms linked to T2DM progression and complications development have been linked to senescence and SASP, that is, oxidative stress and endoplasmic reticulum (ER) stress. Here we review the latest data connecting oxidative and ER stress with the SASP in the context of aging and T2DM, with emphasis on endothelial cells (ECs) and endothelial dysfunction. Moreover, since current medical practice is insufficient to completely suppress the increased death rate of diabetic patients, we propose a SASP-centered view of T2DM as a futuristic therapeutic option, possibly opening new prospects by moving the attention from one-organ studies of diabetes complications to a wider targeting of the aging process.
| Original language | English |
|---|---|
| Article number | 1810327 |
| Journal | Oxidative Medicine and Cellular Longevity |
| Volume | 2016 |
| DOIs | |
| Publication status | Published - 2016 |
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ASJC Scopus subject areas
- Cell Biology
- Ageing
- Biochemistry
Cite this
"Inflammaging" as a Druggable Target : A Senescence-Associated Secretory Phenotype - Centered View of Type 2 Diabetes. / Prattichizzo, F.; De Nigris, Valeria; La Sala, Lucia; Procopio, Antonio; Olivieri, Fabiola; Ceriello, Antonio.
In: Oxidative Medicine and Cellular Longevity, Vol. 2016, 1810327, 2016.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - "Inflammaging" as a Druggable Target
T2 - A Senescence-Associated Secretory Phenotype - Centered View of Type 2 Diabetes
AU - Prattichizzo, F.
AU - De Nigris, Valeria
AU - La Sala, Lucia
AU - Procopio, Antonio
AU - Olivieri, Fabiola
AU - Ceriello, Antonio
PY - 2016
Y1 - 2016
N2 - Aging is a complex phenomenon driven by a variety of molecular alterations. A relevant feature of aging is chronic low-grade inflammation, termed "inflammaging." In type 2 diabetes mellitus (T2DM), many elements of aging appear earlier or are overrepresented, including consistent inflammaging. T2DM patients have an increased death rate, associated with an incremented inflammatory score. The source of this inflammation is debated. Recently, the senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammaging in both aging and T2DM. Different pathogenic mechanisms linked to T2DM progression and complications development have been linked to senescence and SASP, that is, oxidative stress and endoplasmic reticulum (ER) stress. Here we review the latest data connecting oxidative and ER stress with the SASP in the context of aging and T2DM, with emphasis on endothelial cells (ECs) and endothelial dysfunction. Moreover, since current medical practice is insufficient to completely suppress the increased death rate of diabetic patients, we propose a SASP-centered view of T2DM as a futuristic therapeutic option, possibly opening new prospects by moving the attention from one-organ studies of diabetes complications to a wider targeting of the aging process.
AB - Aging is a complex phenomenon driven by a variety of molecular alterations. A relevant feature of aging is chronic low-grade inflammation, termed "inflammaging." In type 2 diabetes mellitus (T2DM), many elements of aging appear earlier or are overrepresented, including consistent inflammaging. T2DM patients have an increased death rate, associated with an incremented inflammatory score. The source of this inflammation is debated. Recently, the senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammaging in both aging and T2DM. Different pathogenic mechanisms linked to T2DM progression and complications development have been linked to senescence and SASP, that is, oxidative stress and endoplasmic reticulum (ER) stress. Here we review the latest data connecting oxidative and ER stress with the SASP in the context of aging and T2DM, with emphasis on endothelial cells (ECs) and endothelial dysfunction. Moreover, since current medical practice is insufficient to completely suppress the increased death rate of diabetic patients, we propose a SASP-centered view of T2DM as a futuristic therapeutic option, possibly opening new prospects by moving the attention from one-organ studies of diabetes complications to a wider targeting of the aging process.
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UR - http://www.scopus.com/inward/citedby.url?scp=84975318302&partnerID=8YFLogxK
U2 - 10.1155/2016/1810327
DO - 10.1155/2016/1810327
M3 - Review article
VL - 2016
JO - Oxidative Medicine and Cellular Longevity
JF - Oxidative Medicine and Cellular Longevity
SN - 1942-0900
M1 - 1810327
ER -