Artemisinin: An Anti-Leishmania Drug that Targets the Leishmania Parasite and Activates Apoptosis of Infected Cells.
Arch Med Res
; 55(6): 103041, 2024 Sep.
Article
en En
| MEDLINE
| ID: mdl-38996535
ABSTRACT
Leishmaniasis is a relevant disease worldwide due to its presence in many countries and an estimated prevalence of 10 million people. The causative agent of this disease is the obligate intracellular parasite Leishmania which can infect different cell types. Part of its success depends on its ability to evade host defense mechanisms such as apoptosis. Apoptosis is a finely programmed process of cell death in which cells silently dismantle and actively participate in several processes such as immune response, differentiation, and cell growth. Leishmania has the ability to delay its initiation to persist in the cell. It has been well documented that different Leishmania species target different pathways that lead to apoptosis of cells such as macrophages, neutrophils, and dendritic cells. In many cases, the observed anti-apoptotic effect has been associated with a significant reduction in caspase-3 activity. Leishmania has also been shown to target several pathways involved in apoptosis such as MAPK, PI3K/Akt, and the antiapoptotic protein Bcl-xL. Understanding the strategies used by Leishmania to subvert the defense mechanisms of host cells, particularly apoptosis, is very relevant for the development of therapies and vaccines. In recent years, the drug artemisinin has been shown to be effective against several parasitic diseases. Its role against Leishmania may be promising. In this review, we provide important aspects of the disease, the strategies used by the parasite to suppress apoptosis, and the role of artemisinin in Leishmania infection.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Leishmaniasis
/
Apoptosis
/
Artemisininas
/
Leishmania
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Arch Med Res
Asunto de la revista:
MEDICINA
Año:
2024
Tipo del documento:
Article
País de afiliación:
México
Pais de publicación:
Estados Unidos