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Importantly, lipid bodies contribute to the establishment of the M2 macrophage phenotype during Leishmania infection by serving as precursors for lipid mediators that regulate both inflammatory and anti-inflammatory activities through omega-3 and omega-6 pathways ( Table 1 )

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These therapies display higher efficiency compared to classical senolytic drugs (BCL-2 or tyrosine kinase inhibitors) but for some of them, such as NA + /K + ATPase inhibitors, clinical development could be complex in the light of strong cardiotoxicity associated with this class of molecules