Role of advanced glycation end products (AGEs) in chronic inflammatory diseases.

Oggetto:

Role of advanced glycation end products (AGEs) in chronic inflammatory diseases.

Oggetto:

Academic year 2019/2020

Teacher

Prof. Manuela Aragno (Titolare del corso)

Teaching period

Da definire

Type

Seminario

Credits/Recognition

Delivery

A distanza

Language

Inglese

Oggetto:

Course objectives

The main aim of the present activity is to provide to PhD students recent emerging evidence on
the role of AGEs, accumulating in tissues in physiological and pathological conditions, in the development of a chronic inflammatory status which contributes to the pathogenesis of many relevant progressive and degenerative diseases.

Oggetto:

Course delivery

Two seminars given by lecturers expert in the proposed field (Prof. Manuela Aragno, Prof.
Massimo Collino, Dr. Raffaella Mastrocola, University of Turin; to be confirmed: Prof. Casper Schalkwijk, University of Maastricht, The Netherland) based on the proposed readings to give the possibility of a better comprehension of the specific issue.

The lectures will be interactive and PhD students will be asked over the speech to try to connect the specific information given on the role of AGEs in pathogenesis of many diseases to the previously known general concepts in pathology. At the end the lectures will be also open for discussion.

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Learning assessment methods

At the end of each lecture, a multiple choice questionnaire will be asked to be filled out to evaluate the efficacy of teaching.

Oggetto:

Program

The recent scientific literature reports a growing body of evidence on the multiple cellular signaling pathways affected by AGEs, involved not only in the induction of oxidative stress and inflammation, but also in the modulation of several metabolic pathways, such as the lipid and sphingolipid metabolism. In the past decades AGEs have been widely investigated for their role in the development of type1 diabetes complications, in particular through the induction of vascular damage. It is now known that AGEs participate also in the development of many chronic inflammatory diseases due to their accumulation in tissues as consequence of the modern dietary habits, characterized by the consumption of both sugarsand saturated fats-rich foods and highly processed foods, responsible for the endogenous and exogenous production of AGEs, respectively. In this perspective, the “glycative stress” is increasingly being recognized as an important underlying pathogenic mechanism for chronic inflammatory diseases.

The teaching activity will be divided into two lectures:

The first will provide information on the biochemical mechanisms of AGEs formation from reactive sugars or lipids and proteins. The different sources of endogenous and exogenous AGEs production will be described, as well as the main AGEs-detoxifying systems. The direct (protein glycation) and indirect (receptor-mediated) mechanisms by which AGEs can exert their detrimental effects on cells and tissues will be illustrated.
In the second lecture an overview of the most recent findings on AGEs involvement in the pathogenesis of different chronic progressive and degenerative diseases will be introduced. In particular, evidence from the literature on the contribution of AGEs and AGEs-related signaling pathways in the development of metabolic diseases, such as obesity and insulin resistance, and the associated cardiovascular and liver diseases, neurodegenerative diseases, atherosclerosis, and kidney diseases, will be reported.

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