SST2Somatostatin Receptor Subtype 2
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IL-33 initiates its signalling pathway by binding to the ST2 receptor, or also known as IL-1R4, with variants which are comprised of ST2L, sST2, ST2V, and ST2LV [1, 4-7].
Blood samples for the evaluation of total, LDL, and HDL cholesterol; triglycerides; glucose; creatinine; serum albumin; uric acid; natrium; potassium; sST2 and NTproBNP were collected in the morning, after overnight fasting and after a period of 5-10-minute rest.
In patients with chronic HF episodes, sST2 acts as a predictor of both all-cause and cardiovascular death [15].
One of these plasma aliquots was used for determination of IL-6, NT-proBNP, hs-cTnT, and sST2. All patient samples were measured in 1 batch approximately 1 month after the recruitment period.
Elevated sST2 which can function as a decoy receptor of IL-33 could be another factor that contributed to the decreased levels of IL-33 observed in PE.
Therefore, considerable efforts have been made to broaden the range of biomarkers, and there was a remarkable increase in the number of HF biomarkers after the year 2001.[sup][7] Among all these candidate markers, soluble suppression of tumorigenicity-2 (sST2) had been regarded as the promising one.[sup][8],[9]
Markers of matrix and cellular remodeling, including collagen propeptides and degradation products, matrix metalloproteinases and their inhibitors, as well as markers that also play a role in the immune system, including growth-differentiation factor 15 (GDF-15), sST2, and galectin-3 have been evaluated as prognostic biomarkers in stable IHD.
In addition, CST was demonstrated to bind sst2, and both preproCST and sst2 are upregulated during macrophage differentiation and after LPS stimulation, suggesting CST might be an endogenous ligand for sst2 in the human immune system [163, 164].
sST2, also released under conditions of mechanical stress and myocyte injury and death appears to act as a "decoy" receptor for IL-33, preventing its binding to ST2L, leading to a circumstance favoring myocardial cell death and ventricular fibrosis and remodeling.
ST2 protein exists in at least 3 isoforms through diverse splicing: a transmembrane form (ST2L), a soluble form (sST2), and a novel variant [7].
Finally, we adjusted for other promising novel biomarkers such as estimated glomerular filtration rate [eGFR; cystatin C-based Chronic Kidney Disease Epidemiology Collaboration (CKDEPI) formula], and finally for sST2, growth differentiation factor 15 (GDF-15), NT-proBNP, and hs-troponin I as they became increasingly available in clinical practice.
ST2 is expressed on the surface of various cellular types, and its gene has three splicing variants, two of which are physiologically important: a soluble variant of ST2 (sST2) and a surface-attached form (ST2L) [3, 4].