AGE RAGE Pathways: Cardiovascular Disease and Oxidative Stress

Author:

Sharma Neeraj1,Kumar Pavan2,Shukla Karuna Shanker3,Maheshwari Shubhrat4

Affiliation:

1. Department of Pharmacy, Bhagwant University, Ajmer, India

2. Ph.D scholar of Department of Pharmacy, Bhagwant University, Ajmer, India

3. Goel Institute of Pharmaceutical Sciences, Uttar Pradesh, Luckow, India

4. Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Rama University, Kanpur, Uttar Pradesh, India

Abstract

AbstractIt is well established that Advanced Glycation End Products (AGEs) and their receptor (RAGE) are primarily responsible for the development of cardiovascular disease. As a result, diabetic therapy is very interested in therapeutic strategies that can target the AGE-RAGE axis. The majority of the AGE-RAGE inhibitors showed encouraging outcomes in animal experiments, but more information is needed to completely understand their clinical effects. The main mechanism implicated in the aetiology of cardiovascular disease in people with diabetes is oxidative stress and inflammation mediated by AGE-RAGE interaction. Numerous PPAR-agonists have demonstrated favourable outcomes in the treatment of cardio-metabolic illness situations by inhibiting the AGE-RAGE axis. The body’s ubiquitous phenomena of inflammation occur in reaction to environmental stressors such tissue damage, infection by pathogens, or exposure to toxic substances. Rubor (redness), calor (heat), tumour (swelling), colour (pain), and in severe cases, loss of function, are its cardinal symptoms. When exposed, the lungs develop silicotic granulomas with the synthesis of collagen and reticulin fibres. A natural flavonoid called chyrsin has been found to have PPAR-agonist activity as well as antioxidant and anti-inflammatory properties. The RPE insod2+/animals underwent mononuclear phagocyte-induced apoptosis, which was accompanied with decreased superoxide dismutase 2 (SOD2) and increased superoxide generation. Injections of the serine proteinase inhibitor SERPINA3K decreased proinflammatory factor expression in mice with oxygen-induced retinopathy, decreased ROS production, and increased levels of SOD and GSH.

Publisher

Georg Thieme Verlag KG

Subject

Drug Discovery,General Medicine

Reference34 articles.

1. Influence of advanced glycation end-products and AGE-inhibitors on nucleation-dependent polymerization of β-amyloid peptide;G Münch;Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease,1997

2. Advanced glycation end products enhance amyloid precursor protein expression by inducing reactive oxygen species;S Y Ko;Free Radical Biology and Medicine,2010

3. Neuroprotective role of Sirt1 in mammalian models of Huntington’s disease through activation of multiple Sirt1 targets;M Jiang;Nature medicine,2012

4. Interactions between SIRT1 and MAPK/ERK regulate neuronal apoptosis induced by traumatic brain injury in vitro and in vivo;Y Zhao;Experimental neurology,2012

5. SIRT1 activating compounds reduce oxidative stress mediated neuronal loss in viral induced CNS demyelinating disease;R S Khan;Acta neuropathologica communications,2014

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