Table 2. The proteins involved in the pathogenesis of cardiovascular diseases seen in OSA .

OSA, Obstructive Sleep Apnea; SBP, Systolic Blood Pressure; DBP, Diastolic Blood Pressure; AHI, Apnea-Hypopnea Index; LOS, Lowest Oxygen Saturation; VEC, Vascular Endothelial Cell; ODI, Oxygen Desaturation Index; AT-1, Angiotensin-1; AT-2, Angiotensin-2

Reference	Study Design		Year of publication	Sample size (n)	Finding	Comments
Kun Li et al. [33]		Clinical trial	2019	157	Protein YKL-40	Protein YKL-40 was found to be higher in OSA subjects, especially with hypertension. The expression of this protein was significantly associated with SBP, DBP, AHI, and LOS. This protein is involved in inflammation, migration of cells, and tissue remodeling. These causes VEC injury and promote atherosclerosis.
Shuhui Wang et al. [2]		Observational	2018	35	Matrix Metalloproteinase-9 (MMP-9)	Hypoxia in OSA leads to the release of MMP-9 protein, which leads to VEC injury via the hypoxia-MMP-9-β2AR (beta2-adrenergic receptor) signaling axis.
Xiuping Yang et al. [34]		Observational	2018	60	Protein miRNA dysregulation	Dysregulated miRNA proteins were seen in OSA patients, possibly targeting genes involved in the metabolism and regulation of endothelial cells.
Macy M S Lui et al. [35]		Observational	2018	98	High-sensitivity troponin l (hsTnI) and C-Reactive Protein (CRP)	Newly diagnosed asymptomatic patients with OSA had increased levels of hsTnI and CRP, depending on their AHI and ODI that represented stable or subclinical cardiac injury and the role of inflammation in VEC injury, respectively.
Rami N Khayat et al.  [18]			2018	21	AT-1 and AT-2 expressions	Upregulation of AT-1 and AT-2 is observed in VEC injury. OSA subjects with no-to-minimum cardiovascular risk were found to have increased expression of AT-1 and AT-2. Such changes could be the major contributing factor for cardiovascular disease.
Vahid Mohsenin et al. [36]		Observational	2011	22	Soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng)	sFlt-1 and sEng are antiangiogenic proteins that cause endothelial dysfunction. It was increased in severe OSA in response to hypoxic stress, especially in patients with hypertension.