ChemInform Abstract: Optimization of 2-Cyano-pyrimidine Inhibitors of Cathepsin K: Improving Selectivity over hERG.

ChemInform ◽  
2011 ◽  
Vol 42 (7) ◽  
pp. no-no
Author(s):  
Zoran Rankovic ◽  
et al. et al.
Keyword(s):  
Cathepsin K ◽  
Abstract Optimization

Knochenumbaumarker

2015 ◽  
Vol 24 (04) ◽  
pp. 215-218
Author(s):  
B. Obermayer-Pietsch ◽  
V. Schwetz
Keyword(s):  
Cathepsin K ◽  
Alkalische Phosphatase ◽  
Compliance Monitoring ◽  
Saure Phosphatase

ZusammenfassungKnochenumbauparameter können zusätzliche Informationen zur Abschätzung der Dynamik des Knochenstoffwechsels in der Osteoporosediagnostik nebst Knochendichte, den klinischen Daten und Routine-Laborparametern liefern. Zu den Aufbaumarkern des Knochenstoffwechsels zählen Prokollagen Typ 1 N-terminales Propeptid (P1NP), die knochenspezifische alkalische Phosphatase (bALP) und Osteokalzin (OC), zu den Abbaumarkern des Knochenstoffwechsels gehören Pyridinolin (PYD) und Desoxypyridinolin (DPD), N-terminales Kollagen-Typ-I-Telopeptid (NTX) und C-terminales Kollagen-Typ-ITelopeptid (CTX), β-CrossLaps (β-CTX), die Tartrat-resistent saure Phosphatase (TRAP5b) sowie Cathepsin K. Das Einsatzgebiet liegt vor allem in der Verlaufsbeurteilung nach Einleitung einer Osteoporosetherapie und im Compliance-Monitoring. Knochenumbaumarker stellen jedoch derzeit keine alleinige Entscheidungsgrundlage zur Initiierung einer Therapie dar. In der Hämatoonkologie scheinen hohe Knochenabbaumarker mit einem höheren Rezidivrisiko bzw. einem höheren Risiko für skelettassoziierte Ereignisse verbunden zu sein.

Cathepsin K

2020 ◽  
Author(s):  
Keyword(s):  
Cathepsin K

Results of study of biochemical markers of bone metabolism in men with coronary heart disease

2020 ◽  
pp. 39-43
Author(s):  
A. V. Voronkina ◽  
T. A. Raskina ◽  
M. V. Letaeva ◽  
Yu. V. Averkieva ◽  
O. S. Malyshenko ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Bone Formation ◽  
Bone Metabolism ◽  
Biochemical Markers ◽  
Coronary Atherosclerosis ◽  
Cathepsin K ◽  
Arterial Calcification ◽  
Mineral Density ◽  
Bone Remodeling Markers

The development of atherosclerosis is closely related to the calcification of the vessel intima and fibrous plaques, being a complex and multifactorial process, in which the markers of bone formation and resorption play an important role. Objective. To study the biochemical markers of bone metabolism in men with stable coronary heart disease (CHD). Material and methods. The study included 102 men with verified CHD. Data were evaluated by densitometry, coronary angiography, multispiral computed tomography, color duplex scanning of brachiocephalic arteries, serum lipids (total cholesterol, triglycerides [TG], high-density [LHD] and low-density lipoprotein cholesterol), concentrationsin the blood of osteocalcin (OC), bone alkaline phosphatase (BAP), cathepsin K and C-telopeptides (CTx). Results. Concentrations of BAP, cathepsin K and CTx in patients with CHD were significantly higher than in men without CHD. The concentration of OC in men with normal bone mineral density was significantly lower than in patients with osteopenic syndrome. There was a direct correlation between OC and antiatherogenic HDL cholesterol and the inverse correlation between OC and TG, CTx and TG. There was no correlation between the level of bone remodeling markers and coronary artery (CA) lesion variant and the severity of coronary atherosclerosis on SYNTAX scale. The correlation analysis did not reveal the connection of biochemical markers of bone metabolism with the severity of coronary atherosclerosis and calcification and thickness of intima-media complex of carotid arteries. Absolute values of bone formation indices (BAP, OC) were significantly higher in patients with severe СA calcification than in patients without signs of calcification. Summary. Increased rates of osteogenesis and osteoresorption characterize the accelerated process of bone metabolism and indicate in favor of high rates of bone loss in men with CHD, which confirms the likelihood of common pathophysiological mechanisms of bone resorption and arterial calcification.

Enhanced load adaptation in long bone of cathepsin K-deficient mice

2014 ◽  
Author(s):  
Nicolas Bonnet ◽  
Lee Duong ◽  
Serge Ferrari
Keyword(s):  
Cathepsin K ◽  
Long Bone ◽  
Deficient Mice

scholarly journals Cathepsin K: A Novel Diagnostic and Predictive Biomarker for Renal Tumors

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2441
Author(s):  
Anna Caliò ◽  
Matteo Brunelli ◽  
Stefano Gobbo ◽  
Pedram Argani ◽  
Enrico Munari ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Therapy Response ◽  
Cathepsin K ◽  
Mtor Inhibitors ◽  
Predictive Marker ◽  
Predictive Biomarker ◽  
Renal Tumors ◽  
Epithelioid Angiomyolipoma

Cathepsin K is a papain-like cysteine protease with high matrix-degrading activity. Among several cathepsins, cathepsin K is the most potent mammalian collagenase, mainly expressed by osteoclasts. This review summarizes most of the recent findings of cathepsin K expression, highlighting its role in renal tumors for diagnostic purposes and as a potential molecular target. Indeed, cathepsin K is a recognized diagnostic tool for the identification of TFE3/TFEB-rearranged renal cell carcinoma, TFEB-amplified renal cell carcinoma, and pure epithelioid PEComa/epithelioid angiomyolipoma. More recently, its expression has been observed in a subgroup of eosinophilic renal neoplasms molecularly characterized by TSC/mTOR gene mutations. Interestingly, both TSC mutations or TFE3 rearrangement have been reported in pure epithelioid PEComa/epithelioid angiomyolipoma. Therefore, cathepsin K seems to be a downstream marker of TFE3/TFEB rearrangement, TFEB amplification, and mTOR pathway activation. Given the established role of mTOR inhibitors as a pharmacological option in renal cancers, cathepsin K could be of use as a predictive marker of therapy response and as a potential target. In the future, uropathologists may implement the use of cathepsin K to establish a diagnosis among renal tumors with clear cells, papillary architecture, and oncocytic features.

scholarly journals Inflammation in the Human Periodontium Induces Downregulation of the α1- and β1-Subunits of the sGC in Cementoclasts

2021 ◽  
Vol 22 (2) ◽  
pp. 539
Author(s):  
Yüksel Korkmaz ◽  
Behrus Puladi ◽  
Kerstin Galler ◽  
Peer W. Kämmerer ◽  
Agnes Schröder ◽  
...  
Keyword(s):  
Protein Expression ◽  
Alveolar Bone ◽  
Soluble Guanylyl Cyclase ◽  
Cathepsin K ◽  
Staining Intensity ◽  
Cyclic Guanosine Monophosphate ◽  
Heme Iron ◽  
Guanosine Monophosphate ◽  
Independent Manner ◽  
Periodontal Tissues

Nitric oxide (NO) binds to soluble guanylyl cyclase (sGC), activates it in a reduced oxidized heme iron state, and generates cyclic Guanosine Monophosphate (cGMP), which results in vasodilatation and inhibition of osteoclast activity. In inflammation, sGC is oxidized and becomes insensitive to NO. NO- and heme-independent activation of sGC requires protein expression of the α1- and β1-subunits. Inflammation of the periodontium induces the resorption of cementum by cementoclasts and the resorption of the alveolar bone by osteoclasts, which can lead to tooth loss. As the presence of sGC in cementoclasts is unknown, we investigated the α1- and β1-subunits of sGC in cementoclasts of healthy and inflamed human periodontium using double immunostaining for CD68 and cathepsin K and compared the findings with those of osteoclasts from the same sections. In comparison to cementoclasts in the healthy periodontium, cementoclasts under inflammatory conditions showed a decreased staining intensity for both α1- and β1-subunits of sGC, indicating reduced protein expression of these subunits. Therefore, pharmacological activation of sGC in inflamed periodontal tissues in an NO- and heme-independent manner could be considered as a new treatment strategy to inhibit cementum resorption.

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