Where cystatin C acts: inside or outside of the plaque

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LETTER TO THE EDITOR

Where cystatin C acts: inside or outside of the plaque Ertan Yetkin 1

&

Bilal Cuglan 2 & Hasan Turhan 1 & Kenan Yalta 3

Received: 19 April 2020 / Accepted: 21 June 2020 # Fondazione Società Italiana di Neurologia 2020

Dear Editor, We have read the impressive article recently published by Ren et al. evaluating the plasma cystatin C (Cyst C) in patients with acute ischemic stroke (AIS) and carotid stenosis [1]. Briefly, they have divided the patients into two groups based on their plasma Cyst C levels and assessed their relation with the degree of carotid stenosis, plaque burden, and morphology. The degree of atherosclerosis, the severity of plaques, and stenosis of the common carotid artery (CCA) of patients with AIS have been found to be significantly higher in the patients with high cystatin C levels. They have concluded that Cyst C levels are strongly correlated with symptomatic CCA stenosis and the rate of unstable plaques. We would like to make additional comments regarding the role of Cyst C in atherosclerosis. The complex and mutual interaction both in circulation and at the tissue level in between the cathepsin (Cat) proteases and their most potent abundant inhibitor Cyst C have gained an increasing interest regarding the pathophysiology of atherosclerosis and dilating vascular diseases as well. The eventual effects of Cyst C activity in the vascular structure are merely determined by Cat proteases. Histopathological studies have shown that increased cysteine protease expression and decreased expression of the endogenous inhibitor Cyst C are in favor of matrix degradation in atherosclerotic tissue and wall of abdominal aortic aneurysms [2, 3]. It is of noteworthy that Cyst C and cathepsin enzymes have also been implicated not only in the pathogenesis obstructive atherosclerotic disease but also in the pathogenesis of dilating vascular disease [3–5]. On the

* Ertan Yetkin [email protected] 1

Department of Cardiology, Istinye University Faculty of Medicine, Istanbul, Turkey

2

Department of Cardiology, Beykent University Faculty of Medicine, Istanbul, Turkey

3

Department of Cardiology, Trakya University Faculty of Medicine, Edirne, Turkey

contrary of higher expression of cathepsin proteases and lower expression of Cyst C in atherosclerotic tissue, higher plasma Cyst C levels have shown to be associated with higher carotid intima-media thickness, diffuse coronary artery disease, and more frequent occurrence of triple vessel disease. Similarly, plasma Cat S and Cyst C are higher in patients with unstable angina than those with stable angina pectoris [2]. Moreover, plasma Cyst C has shown a positive correlation with the plaque area and plaque burdening in unstable angina pectoris but not in stable angina pectoris [2]. It has been presumed that higher plasma levels of Cyst C may reflect the counterbalancing effects of the vessel wall in response to increased elastolytic activity [3]. It has also been postulated that high plasma cystatin C levels might be due to increased infla