|LETTER TO THE EDITOR
|Year : 2022 | Volume
| Issue : 2 | Page : 125-126
The Future Role of Galectin-3 in COVID-19 Era
I Made Gede Widnyana1, Marilaeta Cindryani2, Ni Made Ayu Wulan Sari3
1 Department of Anesthesiology and Intensive Care, Udayana University, Bali, Indonesia
2 Department of Anesthesiology and Intensive Care, University of Indonesia, Jakarta, Indonesia
3 Department of Cardiology, Sanglah General Hospital, Bali, Indonesia
|Date of Submission||02-Feb-2022|
|Date of Decision||10-Mar-2022|
|Date of Acceptance||10-Mar-2022|
|Date of Web Publication||09-May-2022|
Department of Anesthesiology and Intensive Care, University of Indonesia, Jl.Salemba Raya No. 6, Jakarta Pusat 10430
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Widnyana I M, Cindryani M, Sari NM. The Future Role of Galectin-3 in COVID-19 Era. Bali J Anaesthesiol 2022;6:125-6
Galectin-3 is a biomarker that has recently gained its fame in the cardiovascular field. It was approved by the Food and Drug Administration (FDA) as a marker for risk stratification in patients with heart failure in 2014. Galectin-3 plays a role in inflammatory processes such as neutrophil activation and adhesion, opsonization of neutrophils, and mast cell activation. The chronic inflammatory process will cause damage and loss of tissue structure and result in fibrogenesis where it will bridge the acute inflammatory process and the fibrosis that occurs.
As a member of the B-galactoside binding lectin group, it has a molecular weight of 30,000 kDa. Initially, the lectin encoded by the LGALS3 gene was known by many names, including MAC-2 and then CBP-35, lectin L-29, L-34, CBP-30, advanced glycation end-product receptor 3, lectin, galactoside-binding soluble protein, and so on, only later to acquire a definitive identity as Galectin-3. According to several experimental tests conducted on mice, it turned out that Galectin-3 is not only expressed by epithelial cells and myeloid types, but also in various cell types such as cells of the small intestine, colon, cornea, lung, kidney, thymus, and heart cells. In addition, there are many data that Galectin-3 is involved in the immune response, such as in neutrophils, eosinophils, basophils, and mast cells.
Galectin-3 roles have been explored mostly in cardiovascular disease such as atherosclerosis. Atherosclerosis is a proliferative inflammatory response due to injury to the tunica intima. Recent studies have shown that macrophages are recognized as the main inflammatory mediator cells in the atheroma plaque which will cause intima remodeling, subsequent immune response, and activation of scavenging function. From a study of specimen analysis of carotid endarterectomy, limb amputations, and thoracic aorta from autopsies of trauma victims, positive staining for Gal-3 was obtained in the fat core or areas near fibrosis, neovascularization, calcification, bleeding, or thrombosis. Especially in the carotid or lower extremity arteries, foam cells are the most frequently Galectin-3 positive cells. Mononuclear cells and foam cells with Galectin-3 are also frequently present in the subendothelium and sometimes at the site of thrombosis.
Galectin-3 is more associated with diseases such as the incidence of myocardial infarction according to their pathobiological formation involved in the inflammatory and fibrotic processes, although they are still under investigation in vitro or in animals. Circulating levels of Galectin-3 were found to be associated with a history of ischemic heart disease, but they found no association with acute myocardial infarction, Troponin I, high-sensitivity C-reactive protein, left ventricular (LV) volume, and LV ejection fraction. Another meta-analysis reported that Galectin-3 was found to be slightly able to predict the outcome of patients with myocardial infarction but there was no significant relationship between its level and the size of the infarct that occurred. Another study showed that Galectin-3 was shown to have an independent relationship with LV end-diastolic volume (r=0.808; P < 0.001) in patients with acute myocardial infarction undergoing percutaneous coronary intervention.
In the pandemic era, it is already known that COVID-19 infection will have an impact on excessive inflammatory reactions throughout the body, which will facilitate the fibrosis process due to activation of the Gal-3-macrophage-fibroblast axis. The failure or dysfunction of the heart that occurs is not only caused by the proinflammatory activation, but also from the overactivation of the sympathetic nerves, the failure of the respiratory system which also causes heart failure due to heart–lung interaction, and the possibility of direct infection or necrosis of heart myocytes.
Based on heart dysfunction pathophysiology explained by Abboud and Januzzi in 2020, Galectin-3 could provide assistance in determining management and therapy related to the continued effects of COVID-19 infection, which are usually focussed on lungs and mechanical ventilation. The systemic inflammatory response that occurs in COVID-19 not only affects the lungs but also causes dysfunction in the heart that can lead to death. Increased risk of myocardial infection and heart failure are two major heart dysfunctions that would take place in COVID-19. Even though Tian et al. in 2020 have mentioned in their research that more clinical trials and large-scale trials are needed to further confirm the relationship between the Galectin-3 expression and the incidence of myocardial infarction, those recent studies have opened wider opportunities for thorough exploration of main contributors to morbidities in COVID-19.
Galectin-3 could serve as a potential choice of biomarker of heart dysfunction in COVID-19 based on its multifunctional purpose and physiological availability throughout the inflammatory-fibrosis process. Further researches and studies are suggested to confirm its benefit as a future diagnostic marker in COVID-19.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
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