Garza-Campos A, Prieto-Correa JR, Domínguez-Rosales JA, Hernández-Nazará ZH. Implications of receptor for advanced glycation end products for progression from obesity to diabetes and from diabetes to cancer. World J Diabetes 2023; 14(7): 977-994 [PMID: 37547586 DOI: 10.4239/wjd.v14.i7.977]
Corresponding Author of This Article
Zamira Helena Hernández-Nazará, MD, PhD, Departamento de Biología Molecular y Genómica, Instituto de Investigación en Enfermedades Crónico-Degenerativas, Universidad de Guadalajara, Sierra Mojada 950, Col. Independencia C.P. 44350, Guadalajara 44340, Jalisco, Mexico. zamirahelena@yahoo.com.mx
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Jul 15, 2023; 14(7): 977-994 Published online Jul 15, 2023. doi: 10.4239/wjd.v14.i7.977
Implications of receptor for advanced glycation end products for progression from obesity to diabetes and from diabetes to cancer
Andrea Garza-Campos, José Roberto Prieto-Correa, José Alfredo Domínguez-Rosales, Zamira Helena Hernández-Nazará
Andrea Garza-Campos, José Roberto Prieto-Correa, Programa de Doctorado en Ciencias en Biología Molecular en Medicina, Universidad de Guadalajara, Guadalajara 44340, Jalisco, Mexico
Andrea Garza-Campos, José Roberto Prieto-Correa, José Alfredo Domínguez-Rosales, Zamira Helena Hernández-Nazará, Departamento de Biología Molecular y Genómica, Instituto de Investigación en Enfermedades Crónico-Degenerativas, Universidad de Guadalajara, Guadalajara 44340, Jalisco, Mexico
Author contributions: Garza-Campos A and Prieto-Correa JR contributed to the writing, reviewing, and editing of the manuscript; Prieto-Correa JR and Domínguez-Rosales JA prepared the table; Garza-Campos A and Hernández-Nazará ZH prepared the figures; Domínguez-Rosales JA contributed to the writing and performed the majority of the reviewing and editing of the manuscript; Hernández-Nazará ZH and Domínguez-Rosales JA conceptualized the study and designed the outline for the paper; Hernández-Nazará ZH wrote the first draft; and all authors read and approved the final manuscript.
Supported bythe Founding Proyectos de Impulso a la Investigación to Hernandez-Nazara ZH from Universidad de Guadalajara, Mexico, No. PIN 2020-I.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zamira Helena Hernández-Nazará, MD, PhD, Departamento de Biología Molecular y Genómica, Instituto de Investigación en Enfermedades Crónico-Degenerativas, Universidad de Guadalajara, Sierra Mojada 950, Col. Independencia C.P. 44350, Guadalajara 44340, Jalisco, Mexico. zamirahelena@yahoo.com.mx
Received: January 9, 2023 Peer-review started: January 9, 2023 First decision: January 17, 2023 Revised: January 31, 2023 Accepted: April 17, 2023 Article in press: April 17, 2023 Published online: July 15, 2023 Processing time: 184 Days and 15.6 Hours
Abstract
Obesity and type 2 diabetes mellitus (T2DM) are chronic pathologies with a high incidence worldwide. They share some pathological mechanisms, including hyperinsulinemia, the production and release of hormones, and hyperglycemia. The above, over time, affects other systems of the human body by causing tissue hypoxia, low-grade inflammation, and oxidative stress, which lay the pathophysiological groundwork for cancer. The leading causes of death globally are T2DM and cancer. Other main alterations of this pathological triad include the accumulation of advanced glycation end products and the release of endogenous alarmins due to cell death (i.e., damage-associated molecular patterns) such as the intracellular proteins high-mobility group box protein 1 and protein S100 that bind to the receptor for advanced glycation products (RAGE) - a multiligand receptor involved in inflammatory and metabolic and neoplastic processes. This review analyzes the latest advanced reports on the role of RAGE in the development of obesity, T2DM, and cancer, with an aim to understand the intracellular signaling mechanisms linked with cancer initiation. This review also explores inflammation, oxidative stress, hypoxia, cellular senescence, RAGE ligands, tumor microenvironment changes, and the “cancer hallmarks” of the leading tumors associated with T2DM. The assimilation of this information could aid in the development of diagnostic and therapeutic approaches to lower the morbidity and mortality associated with these diseases.
Core Tip: The receptor for advanced glycation products (RAGE) is involved in every stage of the pathophysiological pathways that lead to the progression of obesity, type 2 diabetes, and cancer. This article provides a focused discussion on the stages of obesity leading to the development of metabolic diseases and provides a broad overview of the contribution of RAGE to the development of diabetes and cancer.
