PAI-1: A Major Player in the Vascular Dysfunction in Obstructive Sleep Apnea?

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI, [2000-

Antifibrinolytic Agents* ; Atherosclerosis*/complications ; Atherosclerosis*/genetics ; Cardiovascular System* ; Sleep Apnea, Obstructive*/complications ; Sleep Apnea, Obstructive*/genetics; Humans ; Plasminogen Activator Inhibitor 1/genetics

Obstructive sleep apnea is a chronic and prevalent condition that is associated with endothelial dysfunction, atherosclerosis, and imposes excess overall cardiovascular risk and mortality. Despite its high prevalence and the susceptibility of CVD patients to OSA-mediated stressors, OSA is still under-recognized and untreated in cardiovascular practice. Moreover, conventional OSA treatments have yielded either controversial or disappointing results in terms of protection against CVD, prompting the need for the identification of additional mechanisms and associated adjuvant therapies. Plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of tissue-type plasminogen activator (tPA) and urinary-type plasminogen activator (uPA), is a key regulator of fibrinolysis and cell migration. Indeed, elevated PAI-1 expression is associated with major cardiovascular adverse events that have been attributed to its antifibrinolytic activity. However, extensive evidence indicates that PAI-1 can induce endothelial dysfunction and atherosclerosis through complex interactions within the vasculature in an antifibrinolytic-independent matter. Elevated PAI-1 levels have been reported in OSA patients. However, the impact of PAI-1 on OSA-induced CVD has not been addressed to date. Here, we provide a comprehensive review on the mechanisms by which OSA and its most detrimental perturbation, intermittent hypoxia (IH), can enhance the transcription of PAI-1. We also propose causal pathways by which PAI-1 can promote atherosclerosis in OSA, thereby identifying PAI-1 as a potential therapeutic target in OSA-induced CVD.

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RF1 AG061824 United States AG NIA NIH HHS; AG061824 United States NH NIH HHS

Keywords: atherosclerosis; endothelial dysfunction; intermittent hypoxia; obstructive sleep apnea; plasminogen activator inhibitor-1

0 (Antifibrinolytic Agents)
0 (Plasminogen Activator Inhibitor 1)

Date Created: 20220528 Date Completed: 20220531 Latest Revision: 20240923

20240923

PMC9141273

10.3390/ijms23105516

35628326