Perspective, Int J Cardiol Res Vol: 12 Issue: 1
Impact of Heparin Binding Protein in Cardiovascular Disease
Received date: 14 February, 2023, Manuscript No. ICRJ-23-91634;
Editor assigned date: 16 February, 2023, PreQC No. ICRJ-23-91634 (PQ);
Reviewed date: 03 March, 2023, QC No. ICRJ-23-91634;
Revised date: 10 March, 2023, Manuscript No. ICRJ-23-91634 (R);
Published date: 20 March, 2023 DOI: 10.4172/2324-8602.1000481.
Citation: Pierson D (2023) Impact of Heparin Binding Protein in Cardiovascular Disease. Int J Cardiol Res 12:1.
Cardiovascular diseases are a significant group of diseases that have a negative impact on quality of life. As a result, their treatment merits further investigation. Heparin Binding Protein (HBP) is a neutrophilderived granulocyte protein. When an infection occurs, neutrophils release HBP, which can result in elevated blood HBP levels. As a result, HBP family members are considered important indicators of infection. However, basic evidence to confirm the possible link between HBP and cardiovascular disease is still lacking. Cardiovascular disease is one of the most common diseases, with a high incidence and mortality rate. Cardiovascular diseases are distinguished by their sudden onset, critical condition, and rapid progression. The most common diseases in clinical practice are atherosclerosis, myocarditis, myocardial infarction, and myocardial ischemia, and the majorities of patients die as a result of misdiagnosis and delayed treatment. Atherosclerosis primarily affects large and medium-sized arteries, with the basic lesions being lipid deposition in the intima, focal fibrosis of the intima, and the formation of atherosclerotic plaques. Myocarditis is a limited or diffuse inflammatory lesion of the myocardium in which inflammatory cells infiltrate the myocardium, causing denaturation and necrosis of adjacent cardiomyocytes.
A myocardial infarction is a disease in which the blood supply to the coronary arteries is interrupted, resulting in extensive myocardial necrosis. Myocardial ischemia is a pathological condition in which the heart's blood perfusion decreases, resulting in a decrease in oxygen supply to the heart and abnormal energy metabolism. As a result, it is critical to identify a representative biomarker that can indicate the occurrence of the aforementioned diseases through plasma levels and changes in protein expression levels in order to improve treatment or even enable prevention. This research has the potential to lead to the development of new therapies for clinical use.
When activated neutrophils adhere to the endothelium or are stimulated by circulating bacterial metabolites, they release HBP. HBP can cause the endothelial cytoskeleton to rearrange, resulting in the destruction of the vascular endothelial barrier, the migration of white blood cells from capillaries to infection sites, and an increase in vascular permeability. HBP has been shown in studies to play an important role in the regulation of the inflammatory response. When monocytes and macrophages are activated, inflammatory mediators such as tumor necrosis factor and interferon are released to amplify the inflammatory response, which is linked to the development of hypotension and circulatory failure.
Patients with acute kidney injury, sepsis, pancreatic diseases, lung injuries, immune system diseases, spontaneous bacterial peritonitis, and other diseases have previously been found to have abnormal HBP plasma levels. However, while these basic clinical experiments provide auxiliary proof of the HBP's role, they do not fully reveal the interaction networks and genetic mechanisms at work. Bioinformatics tools like cytoscape and Metascape to examine the network of interactions between HBP family members in cardiovascular diseases like atherosclerosis, myocarditis, myocardial infarction, and myocardial ischemia. The interaction of HBPs is discussed in light of gene and protein networks identified through bioinformatics analyses in order to elucidate the value of HBPs as novel biomarkers of the severity and prognosis of typical cardiovascular diseases.