In the aetiology of the typical CP wrist joint postures. The substantial individual variation, however, also indicates that this may not be the exclusive mechanism contributing to these wrist postures. Chronic thromboembolic pulmonary hypertension is characterized by continuously increased pulmonary vascular resistance due to unresolved emboli in major pulmonary Dabrafenib arterials and/or pulmonary microvascular remodeling. Recent epidemiology studies showed that the incidence of CTEPH in acute pulmonary thromboembolism survivors was about 2.7%– 8.8%, and 2-year survival in untreated patients with a mean pulmonary artery pressure greater than 50 mmHg was as low as 10%. However, recognition before CTEPH progression is difficult for the insidious onset and lack of effective biomarker of it. MicroRNAs are small endogenous non-coding RNAs that suppress gene expression post-transcriptionally by binding to the “seed sequences” in 39 untranslated regions of target mRNAs. Dysregulation of miRNAs has been found in different diseases and biological processes. Recent studies have shown that miRNAs were involved in pulmonary vascular remodeling and susceptibility of CTEPH, as well as pulmonary arterial smooth muscle cells malproliferation of pulmonary arterial hypertension. Circulating miRNAs, known as stable cell-free miRNAs in serum or plasma, are passively and selectively released to blood by various cells, and may act as transmitter or messenger in cell communication. During disease, aberrantly expressed miRNAs in the diseased cells are released into the circulation, and the circulating miRNA profile is endued with the disease properties. Recently, circulating miRNAs have been extensively studied as potential blood-based biomarkers for disease diagnosis, especially in malignancies and cardiovascular diseases. Plasma miR-134 has been shown to be a specific biomarker for acute pulmonary thromboembolism. Multiple pathophysiologic processes have been reported to contribute to the progression of CTEPH, including imbalance of endothelin-1, nitric oxide and prostacyclin, dysfunction of pulmonary arterial endothelial cells, and malproliferation of PASMCs. ET-1 is a key vasoconstrictor especially in pulmonary circulation, and can cause proliferation of many cells involved in vascular remodeling. ET-1 level was elevated in CTEPH patients, and endothelin receptor antagonists have been applied for CTEPH treatment. Transforming growth factor -b plays important regulatory roles in the balance of cell proliferation and apoptosis. The abnormal activation of TGF-b/transforming growth factor beta receptor 1 signaling was involved in development of idiopathic PAH. Clarify the relationship between candidate miRNAs and these known mechanisms would intensify the recognition of disease pathogenesis. In present study, we demonstrated that CTEPH patients had a differently expressed miRNA profile. And a signature of 17 miRNAs was shown to be related to the disease pathogenesis and gave the diagnostic efficacy of both sensitivity and specificity.0.9. Let-7b, one of the key miRNAs, might be involved in the pathogenesis of CTEPH by affecting ET-1 expression and the migration of PAECs and PASMC.