Levels of cathepsins in acute myocardial infarction

Shalia, Kavita; Mashru, Manoj; Shah, Vinod K.; Soneji, Surendra L; Payannavar, Satchidanand

doi:10.1016/s0019-4832(12)60089-3

Cited by 16 publications

(7 citation statements)

References 17 publications

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“…Nevertheless, in a study from India [25], higher circulating levels of cathepsin B were seen in patients with acute myocardial infarction when compared to controls and one of the inclusion criteria in the CLARICOR trial was previous myocardial infarction (at any point in a six-year period preceding inclusion). Thus, one speculation could be that the risk associated with higher cathepsin B levels in our present paper reflects a more severe myocardial infarction, indicating higher-risk coronary disease.…”

Section: Potential Mechanismsmentioning

confidence: 97%

Cathepsin B and S as markers for cardiovascular risk and all-cause mortality in patients with stable coronary heart disease during 10 years: a CLARICOR trial sub-study

et al. 2018

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Section: Potential Mechanismsmentioning

confidence: 97%

Cathepsin B and S as markers for cardiovascular risk and all-cause mortality in patients with stable coronary heart disease during 10 years: a CLARICOR trial sub-study

et al. 2018

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“…Similar alterations in Cat K and Cys C expression were reported in the later stages of cerebral aneurysm progression ( 33 ). Furthermore, the expression of Cys C and Cat K were significantly decreased and increased respectively, during acute myocardial infarction ( 34 ). Additionally, the expression of Cys C was elevated in the brains of Cat K deficient mice ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

Decreased cathepsin K levels in human atherosclerotic plaques are associated with plaque instability

Zhao

Qin

Wang

et al. 2017

Experimental and Therapeutic Medicine

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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.

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“…This, in turn, degrades the ECM in the weak area of plaque ber cap, thereby destabilizing the plaque and inducing rupture. IFNγpositively modulates myocardial cell necrosis by increasing local nitric oxide synthesis [42][43][44][45].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analyses of potentially common pathogenic networks for primary Sjogren’s syndrome complicated with acute myocardial infarction

Hou

Jiang

et al. 2023

Preprint

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Both primary Sjogren’s syndrome (pSS) and acute myocardial infarction (AMI) are intricately linked to one another. However, their common mechanism is not fully understood. Herein, we examined the underlying network of molecular action associated with the development of this complication.datasets were downloaded from the GEO database, We performed enrichment and protein–protein interaction analyses and screened key genes. To confirm the diagnostic performance for these hub genes, we used external datasets. Transcription factor and microRNA regulatory networks were constructed for the validated hub genes. Finally, drug prediction and molecular docking validation were performed.We identified 51 commonDEGs, many of which were enriched in terms of Inflammation and immune response. five DEGs were found as key hub genes ( IGSF6、MMP9、S100A8, MNDA, and NCF2). They had high diagnostic performance in external datasets. Functional enrichment of these five hub genes showed that they were associated with the adaptive immune response.The Type 1 T helper cell showed the most association among all cell types related to AMI and pSS. we identified 27 common TFs and 20 identical TF-miRNAs. The drugs including Benzo、dexamethasone and NADP were predicted as potential therapeutic agents. Herein, we revealed common networks involving pSS and AMI etiologies. Knowledge of these networks and hub genes can enhance research into their associated mechanism and development of future robust therapy.

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Levels of cathepsins in acute myocardial infarction

Cited by 16 publications

References 17 publications

Cathepsin B and S as markers for cardiovascular risk and all-cause mortality in patients with stable coronary heart disease during 10 years: a CLARICOR trial sub-study

Cathepsin B and S as markers for cardiovascular risk and all-cause mortality in patients with stable coronary heart disease during 10 years: a CLARICOR trial sub-study

Decreased cathepsin K levels in human atherosclerotic plaques are associated with plaque instability

Bioinformatics analyses of potentially common pathogenic networks for primary Sjogren’s syndrome complicated with acute myocardial infarction

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