Enhanced production of reactive oxygen species (ROS) can be linked to various diseases such as diabetes and cardiovascular disease. Heme oxygenase (HO)-1, a cytoprotective heme-degrading enzyme, is upregulated by pathophysiological stimuli that increase oxidative stress. However, the role of heme oxygenase (HO)-1 in post-myocardial infarction (MI) and diabetes has not been comprehensively researched. The intracellular enzyme heme oxygenase-1 (HO-1) catalyzes the oxidation of heme to ferrous iron, carbon monoxide, and biliverdine, which is subsequently converted by biliverdine reductase into bilirubin. The enzymatic reaction can have significant biological effects such as antioxidant, anti-inflammatory, and cytoprotective functions as well as reduced hyperglycemia. The heme oxygenase system also improves the sensitivity of insulin and insulin synthesis of pancreatic beta cells in both type 1 and type 2 experimental models of diabetes. While HO-1 is inducible in response to physiological stress, it is expressed in most tissues under basal conditions at low concentrations. Thus, HO-1 induction is considered an adaptive defence mechanism that helps to defend cells and tissues from damage in many disease settings.

Current studies have shown that HO-1 prevents extrinsic and intrinsic apoptotic pathways in vitro induced by stress. A series of signalling molecules, including autophagus protein, p38 Mitogen-activated kinase protein, transcription protein signal transducer and activator, nuclear factor-kappaB (NF-κB), phosphatidylinositol 3 kinase / Akt etc. have been used in cytoprotection conferred by HO-1. Enhanced HO-1, or pharmaceutical use of HO-end products, provides preclinical models for protection against tissue injury, which include experimental and transplant-associated ischemia reperfusion injury, suggesting potential future therapeutic applications.  

The aim of this Special Issue is to investigate the current trends, advancements, and role of heme oxygenase in diabetes and cardiovascular disease treatment contributing to precision approaches in metabolic disorders. Original research and review articles are welcome. 

Potential topics include but are not limited to the following:

• Pathophysiological role of HO-1 in Diabetes and Cardiovascular diseases 
• Role of HO-1 in the cardiovascular complications of diabetes 
• Mechanisms by which the HO system potentiates signalling/metabolic pathways in cardiometabolic diseases 
• Emerging role of the HO in insulin release, insulin sensitvity, glucose metabolism, oxidative stress and inflammatory responses
• Stimulatory relationship of HO system with inflammatory/oxidative transcription factors and their role in the regulation of cellular metabolism