Increased cathepsin K levels in human atherosclerotic plaques are associated with plaque instability
Corrigendum in: /10.3892/etm.2017.5660
Affiliations: Department of Gerontology, First Hospital, Jilin University, Changchun, Jilin 130021, P.R. China, Department of Cardiology, Jihua General Hospital, Jilin University, Changchun, Jilin 130021, P.R. China, Department of Vascular Surgery, First Hospital, Jilin University, Changchun, Jilin 130021, P.R. China
- Published online on: August 16, 2017 https://doi.org/10.3892/etm.2017.4935
- Pages: 3471-3476
Copyright: © Zhao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Investigating the determinants and dynamics of atherosclerotic plaque instability is a key area of current cardiovascular research. Extracellular matrix degradation from excessive proteolysis induced by enzymes such as cathepsin K (Cat K) is implicated in the pathogenesis of unstable plaques. The current study assessed the expression of Cat K in human unstable atherosclerotic plaques. Specimens of popliteal arteries with atherosclerotic plaques were classified as stable (<40% lipid core plaque area; n=6) or unstable (≥40% lipid core plaque area; n=14) based on histopathological examinations of hematoxylin and eosin stained sections. The expression of Cat K and cystatin C (Cys C) were assessed by immunohistochemical examination and levels of Cat K mRNA were detected by semi‑quantitative reverse transcriptase polymerase chain reaction. Morphological changes including a larger lipid core, endothelial proliferation with foam cells and destruction of internal elastic lamina were observed in unstable atherosclerotic plaques. In unstable plaques, the expression of Cat K protein and mRNA was upregulated, whereas Cys C protein expression was downregulated. The interplay between Cat K and Cys C may underlie the progression of plaques from stable to unstable and the current study indicated that Cat K and Cys C are potential targets for preventing and treating vulnerable atherosclerotic plaque ruptures.