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Angelica Giuliani [1] and Francesco Prattichizzo [2; 3] and Luigina Micolucci [1] and Antonio Ceriello [2; 3; 4] and Antonio Domenico Procopio [1; 5] and Maria Rita Rippo [1]

Academic Editor: Michal A. Rahat

1, Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy, univpm.it

2, IRCCS Multimedica, 20099 Sesto San Giovanni, Italy, multimedica.it

3, Insititut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), C/Rosselló 149-153, 08036 Barcelona, Spain, idibaps.org

4, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain, ciberdem.org

5, Center of Clinical Pathology and Innovative Therapy, Italian National Research Center on Aging (INRCA-IRCCS), Ancona, Italy, inrca.it

Received Sep 29, 2017; Accepted Nov 20, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Aging constitutes the major risk factor for a variety of diseases with a high-incidence in the Western society. Type 2 diabetes (T2DM), metabolic syndrome, cardiovascular diseases (CVD), neurodegenerative diseases, and a plethora of common cancer types share aging as a common risk factor and therefore are often referred as aging-related diseases (ARDs). A pervasive feature of aging is a progressive and chronic state of systemic low-grade inflammation referred as inflammaging [1]. Major ARDs all share a common inflammatory background. The role of various inflammatory molecules—mainly tumor necrosis factor- (TNF-) α, interleukin- (IL-) 1b, IL-6, and transforming growth factor- (TGF-) β—in the promotion or exacerbation of a wide range of ARDs is increasingly emerging [1]. A number of mechanisms, pathways, and cell types have been shown to possibly contribute to inflammaging [2]. Initial hypothesis affirmed that inflammaging was mainly due to the long-lasting exposure to acute and chronic infections and the consequent life-long antigenic burden [3]. However, a long list of sterile potential sources of inflammatory molecules during both the cellular and the organismal aging process has been proposed [2].

The “old” free radical theory of aging (FRTA) states that organisms age because cells accumulate free radical-induced damage over time [4]. One interesting view that coupled FRTA with inflammaging is the oxi-inflammaging theory [5]. Accordingly, excessive or uncontrolled free radical production can induce an inflammatory response, and free radicals are themselves...

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