Modulation of calcium signaling and metabolic pathways in endothelial cells with magnetic fields

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378271%3A_____%2F24%3A00584436" target="_blank" >RIV/68378271:_____/24:00584436 - isvavai.cz</a>

Výsledek na webu

<a href="https://hdl.handle.net/11104/0356498" target="_blank" >https://hdl.handle.net/11104/0356498</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1039/d3na01065a" target="_blank" >10.1039/d3na01065a</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Modulation of calcium signaling and metabolic pathways in endothelial cells with magnetic fields

Popis výsledku v původním jazyce

Calcium signaling plays a crucial role in various physiological processes, including muscle contraction, cell division, and neurotransmitter release. Dysregulation of calcium levels and signaling has been linked to a range of pathological conditions such as neurodegenerative disorders, cardiovascular disease, and cancer. Here, we propose a theoretical model that predicts the modulation of calcium ion channel activity and calcium signaling in the endothelium through the application of either a time-varying or static gradient magnetic field (MF). This modulation is achieved by exerting magnetic forces or torques on either biogenic or non-biogenic magnetic nanoparticles that are bound to endothelial cell membranes. Since calcium signaling in endothelial cells induces neuromodulation and influences blood flow control, treatment with a magnetic field shows promise for regulating neurovascular coupling and treating vascular dysfunctions associated with aging and neurodegenerative disorders. Furthermore, magnetic treatment can enable control over the decoding of Ca signals, ultimately impacting protein synthesis. The ability to modulate calcium wave frequencies using MFs and the MF-controlled decoding of Ca signaling present promising avenues for treating diseases characterized by calcium dysregulation.

Název v anglickém jazyce

Modulation of calcium signaling and metabolic pathways in endothelial cells with magnetic fields

Popis výsledku anglicky

Calcium signaling plays a crucial role in various physiological processes, including muscle contraction, cell division, and neurotransmitter release. Dysregulation of calcium levels and signaling has been linked to a range of pathological conditions such as neurodegenerative disorders, cardiovascular disease, and cancer. Here, we propose a theoretical model that predicts the modulation of calcium ion channel activity and calcium signaling in the endothelium through the application of either a time-varying or static gradient magnetic field (MF). This modulation is achieved by exerting magnetic forces or torques on either biogenic or non-biogenic magnetic nanoparticles that are bound to endothelial cell membranes. Since calcium signaling in endothelial cells induces neuromodulation and influences blood flow control, treatment with a magnetic field shows promise for regulating neurovascular coupling and treating vascular dysfunctions associated with aging and neurodegenerative disorders. Furthermore, magnetic treatment can enable control over the decoding of Ca signals, ultimately impacting protein synthesis. The ability to modulate calcium wave frequencies using MFs and the MF-controlled decoding of Ca signaling present promising avenues for treating diseases characterized by calcium dysregulation.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10610 - Biophysics

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2024

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Nanoscale Advances

ISSN

2516-0230

e-ISSN

2516-0230

Svazek periodika

6

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

20

Strana od-do

1163-1182

Kód UT WoS článku

001151620700001

EID výsledku v databázi Scopus

2-s2.0-85184026738