Implication of advanced glycation end products (Ages) and their receptor (Rage) on myocardial contractile and...

Area of Science:

• Cardiovascular Biology
• Metabolic Disorders
• Molecular Medicine

Background:

• Advanced glycation end products (AGEs) are formed via non-enzymatic sugar reactions with proteins, lipids, and nucleic acids.
• Both endogenous formation and dietary intake contribute to AGE accumulation.
• AGEs impact cardiac cell structure and function, promoting cardiovascular disease progression.

Purpose of the Study:

• To review the role of AGEs in cardiovascular disease development and progression.
• To elucidate the mechanisms by which AGEs induce oxidative stress and inflammation in cardiac cells.
• To highlight AGE-induced mitochondrial dysfunction in the myocardium as a key factor in heart failure.

Main Methods:

• Literature review of studies on AGEs, RAGE signaling, oxidative stress, inflammation, and cardiovascular disorders.
• Analysis of molecular mechanisms linking AGEs to cellular dysfunction.
• Focus on AGEs' impact on mitochondrial function in cardiomyocytes.

Main Results:

• AGEs induce oxidative stress and inflammation via receptor for advanced glycation end products (RAGE) activation.
• RAGE activation upregulates nuclear factor-κB, promoting inflammatory and fibrotic responses.
• AGE accumulation disrupts cardiac cell structure and function, contributing to microvascular and macrovascular complications.

Conclusions:

• AGEs are significant contributors to cardiovascular disease pathogenesis.
• Targeting AGEs and RAGE pathways may offer therapeutic strategies for cardiovascular disorders.
• AGE-induced mitochondrial dysfunction is a critical mechanism underlying heart failure.