Por favor, use este identificador para citar o enlazar este ítem: https://hdl.handle.net/20.500.12008/56395

Título:

How Protein Depletion Balances Thrombosis and Bleeding Risk in the Context of Platelet’s Activatory and Negative Signaling

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Autor:

Montecino-Garrido, Héctor
Trostchansky, Andrés
Espinosa-Parrilla, Yolanda
Palomo, Iván
Fuentes, Eduardo

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Tipo de documento:

Artículo

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Palabras clave:

Activatory
Bleeding
Inhibitory
Platelets
Signaling

Descriptores:

ANIMALES
METABOLISMO
PLAQUETAS
HEMORRAGIA
HEMOSTASIS
HUMANOS
ACTIVACIÓN PLAQUETARIA
TRANSDUCCIÓN DE SEÑAL
TROMBOSIS

Año de publicación:

2024

Contenido:

Resumen:

Platelets are small cell fragments that play a crucial role in hemostasis, requiring fast response times and fine signaling pathway regulation. For this regulation, platelets require a balance between two pathway types: the activatory and negative signaling pathways. Activatory signaling mediators are positive responses that enhance stimuli initiated by a receptor in the platelet membrane. Negative signaling regulates and controls the responses downstream of the same receptors to roll back or even avoid spontaneous thrombotic events. Several blood-related pathologies can be observed when these processes are unregulated, such as massive bleeding in activatory signaling inhibition or thrombotic events for negative signaling inhibition. The study of each protein and metabolite in isolation does not help to understand the role of the protein or how it can be contrasted; however, understanding the balance between active and negative signaling could help develop effective therapies to prevent thrombotic events and bleeding disorders.

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MDPI

EN:

International Journal of Molecular Sciences. 2024;25(18)

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Citación:

Montecino-Garrido H, Trostchansky A, Espinosa-Parrilla Y y otros. How Protein Depletion Balances Thrombosis and Bleeding Risk in the Context of Platelet’s Activatory and Negative Signaling. International Journal of Molecular Sciences [en línea]. 2024;25(18). 27 p.

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Licencia Creative Commons Atribución (CC - By 4.0)
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