Inflammation, Advancing Age and Nutrition by Rahman Irfan; Bagchi Debasis; & Debasis Bagchi

Author:Rahman, Irfan; Bagchi, Debasis; & Debasis Bagchi
Language: eng
Format: epub
Publisher: Elsevier Science
Published: 2013-09-11T16:00:00+00:00

Chapter 15

SIRT1 and Inflammaging in Chronic Obstructive Pulmonary Disease

Jae-Woong Hwang, Isaac K. Sundar, Hongwei Yao and Irfan Rahman, Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY, USA

Abstract

Oxidative stress, chronic inflammation, and cellular senescence are intertwined in the pathogenesis of premature aging, which is considered to be an important contributory factor in driving chronic lung diseases, such as chronic obstructive pulmonary disease (COPD). COPD is a disease of lung inflammaging associated with a rapid decline in lung function. Lung inflammaging in patients with COPD is associated with an increase in the DNA damage response, cellular senescence, and transcription of proinflammatory mediators. SIRT1 regulates inflammaging via regulating FOXO3, p53, and NF-κB, as well as various proteins/coactivators involved in DNA damage and repair. Oxidant/carbonyl stress imposed by cigarette smoke reduces SIRT1 levels and activity, which results in acetylation of target proteins, such as p53, RelA/p65, and FOXO3, thereby leading to increased inflammatory response, cellular senescence, and apoptosis. Targeting lung inflammaging using pharmacological SIRT1 activators or polyphenols is therefore a promising therapeutic intervention for inflammaging in chronic lung diseases including COPD.

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