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Vascular Calcification Regulated by Klotho During Physiological and Pathophysiological Aging

Vaskularna kalcifikacija regulirana Klotho proteinom tijekom fiziološkog i patofiziološkog starenja
Authors: Primc, Davor; Peršić, Viktor; Španjol, Josip; Divković, Dalibor; Kovačević, Miljenko; Pećanić, Sanja; Miletić Gršković, Silvija; +1 Authors

Vascular Calcification Regulated by Klotho During Physiological and Pathophysiological Aging

Abstract

Purpose: The widely spread membrane and soluble Klotho protein plays a pivotal role in vascular calcification by orchestrating calcium/phosphate/magnesium homeostasis mediated by the Klotho/fibroblast growth factor 23 receptor complex. Our aim was to review new scientific data and discuss the role(s) of Klotho in vascular calcification. The basic procedures were to review the literature concerning Klotho and its mechanisms of action during physiological and pathological aging. Main findings: A lack of Klotho shortens the lifespan, increases vascular calcification and the frequency of cardiovascular diseases with multiple organ degeneration and weakness in experimental animal models. In humans, the most prominent decrease of Klotho protein and mRNA is found in patients with chronic kidney disease–mineral and bone disorder (CKD–MBD), which shows accelerated aging due to increased vascular calcification. Additionally, Klotho acts in an endocrine manner participating in different signaling pathways as an anti-inflammatory, antioxidant, anti-fibrotic and anti-aging mediator, preserving vascular structure and function. Principal conclusions: Klotho is a possible early marker for the detection and monitoring of subclinical arterial calcification in patients with CKD–MBD and in the general population.

Svrha studije: Široko rasprostranjen membranski i topivi Klotho protein igra ključnu ulogu u vaskularnoj kalcifikaciji podešavanjem homeostaze kalcija, fosfata i magnezija posredovanog kompleksom Klotho / receptor čimbenika rasta fibroblasta 23. Cilj je bio pregledati nove znanstvene rezultate i raspraviti ulogu Klotho proteina u kalcifikaciji arterija. Osnovni postupci bili su pregled literature o Klotho proteinu i njegovim mehanizmima djelovanja tijekom fiziološkog i patološkog starenja. Glavni nalazi: Nedostatak Klotho proteina odražava se na skraćeni životni vijek, vaskularnu kalcifikaciju i kardiovaskularne bolesti s degeneracijom više organa i slabošću organizma u eksperimentalnim modelima životinja. Najizraženije smanjenje Klotho proteina i mRNA kod ljudi nalazi se u bolesnika s kroničnom bolešću bubrega – mineralnim i koštanim poremećajem (CKD–MBD), koji pokazuju ubrzano starenje zbog povećanih vaskularnih kalcifikacija. Klotho djeluje na endokrini način sudjelujući u različitim signalnim putovima kao protuupalni, antioksidativni i antifibrotični posrednik te protiv starenja koji čuva strukturu i funkciju arterija. Glavni zaključci: Klotho je mogući rani marker za otkrivanje i praćenje subkliničkih arterijskih kalcifikacija u bolesnika s CKD–MBD i u općoj populaciji.

Country
Croatia
Keywords

Hyperphosphatemia, Chronic kidney disease–mineral bone disorder, α-Klotho, Vaskularna kalcifikacija, Kronična bubrežna bolest – mineralni i koštani poremećaj, Hiperfosfatemija, Fibroblast growth factor 23, Vascular calcification, Čimbenik rasta fibroblasta 23

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average