Sarcopenia is a common complication of chronic kidney disease (CKD) and has a detrimental effect on prognosis. Previous studies have explored the role of secondary calciprotein particles (CPP2) in determining the progression of complications and poor outcomes in patients with CKD. However, no study has demonstrated that CPP2 impairs skeletal myogenesis. Our study revealed that CPP2 exposure inhibits skeletal myogenesis by suppressing myotube formation and expression of skeletal muscle-specific myosin heavy chain and actin in human primary myoblasts. Moreover, CPP2 exposure altered the expression patterns of lineage-determinative transcription factors responsible for regulating myotube differentiation marker genes. This study first demonstrated that CPP2 interferes with myoblast differentiation and myotube formation in vitro.
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http://dx.doi.org/10.2220/biomedres.45.173 | DOI Listing |
Kidney Dis (Basel)
December 2024
Department of Nephrology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Background: The bone-vascular axis plays a key role in the pathogenesis of vascular calcification (VC) in patients with chronic kidney disease (CKD). Understanding and managing the role of the bone-vascular axis in CKD-mineral and bone disorder (CKD-MBD) is critical for preventing and treating associated complications, including osteoporosis, arterial calcification, and cardiovascular diseases. This study aimed to comprehensively summarize the role of bone metabolism markers in uremic VC.
View Article and Find Full Text PDFVet J
November 2024
Department of Comparative Biomedical Sciences, Royal Veterinary College, University of London, Royal College Street, London NW1 0TU, United Kingdom.
Fibroblast growth factor-23 (FGF23) is a phosphaturic hormone, discovery of which has transformed our understanding of mineral regulation in healthy mammals, including the cat. It is produced by osteoblasts and osteocytes and its prime role is to regulate phosphate entry into extracellular fluid (from bone and via the gut) and its excretion via the kidney. It interacts with other hormones (calcitriol and parathyroid hormone), inhibiting their activation and secretion respectively and so impacts on calcium as well as phosphate homeostasis.
View Article and Find Full Text PDFJ Atheroscler Thromb
November 2024
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University.
Patients with chronic kidney disease (CKD) have a high incidence of atherosclerotic diseases, such as ischemic heart disease, cerebrovascular disease, and peripheral arterial disease. To prevent the incidence of atherosclerotic cardiovascular disease in patients with CKD, the pathology of arteriosclerosis should be determined. Vascular calcification is a characteristic of arteriosclerosis in patients with CKD.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Experimental Medicine, Research Institute for Complex Issues of Cardiovascular Diseases, 6 Barbarash Boulevard, 650002 Kemerovo, Russia.
Calciprotein particles (CPPs) are essential circulating scavengers of excessive Ca and PO ions, representing a vehicle that removes them from the human body and precludes extraskeletal calcification. Having been internalised by endothelial cells (ECs), CPPs induce their dysfunction, which is accompanied by a remarkable molecular reconfiguration, although little is known about this process's extracellular signatures. Here, we applied ultra-high performance liquid chromatography-tandem mass spectrometry to perform a secretome-wide profiling of the cell culture supernatant from primary human coronary artery ECs (HCAECs) and internal thoracic artery ECs (HITAECs) treated with primary CPPs (CPP-P), secondary CPPs (CPP-S), magnesiprotein particles (MPPs), or Ca/Mg-free Dulbecco's phosphate-buffered saline (DPBS) for 24 h.
View Article and Find Full Text PDFNephrology (Carlton)
December 2024
Service of Nephrology, Ospedale Regionale di Lugano, Ospedale Civico, Ente Ospedaliero Cantonale, Lugano, Switzerland.
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a syndrome commonly observed in subjects with impaired renal function. Phosphate metabolism has been implicated in the pathogenesis of CKD-MBD and according to the phosphorocentric hypothesis may be the key player in the pathogenesis of these abnormalities. As phosphorous is an essential component for life, absorption from the bowel, accumulation and release from the bones, and elimination through the kidneys are all homeostatic mechanisms that maintain phosphate balance through very sophisticated feedback mechanisms, which comprise as main actors: vitamin D (VD), parathyroid hormone (PTH), calciproteins particles (CPPs), fibroblast growth factor-23 (FGF-23) and other phosphatonins and klotho.
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