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2. Transmission-Blocking Strategies for Malaria Eradication: Recent Advances in Small-Molecule Drug Development.

Author

Appetecchia, Federico, Fabbrizi, Emanuele, Fiorentino, Francesco, Consalvi, Sara, Biava, Mariangela, Poce, Giovanna, and Rotili, Dante

Subjects
MOSQUITO vectors, CHEMICAL libraries, MALARIA, MALARIA prevention, PLASMODIUM falciparum, OOCYSTS
Abstract

Malaria drug research and development efforts have resurged in the last decade following the decelerating rate of mortality and malaria cases in endemic regions. The inefficiency of malaria interventions is largely driven by the spreading resistance of the Plasmodium falciparum parasite to current drug regimens and that of the malaria vector, the Anopheles mosquito, to insecticides. In response to the new eradication agenda, drugs that act by breaking the malaria transmission cycle (transmission-blocking drugs), which has been recognized as an important and additional target for intervention, are being developed. These drugs take advantage of the susceptibility of Plasmodium during population bottlenecks before transmission (gametocytes) and in the mosquito vector (gametes, zygotes, ookinetes, oocysts, sporozoites). To date, compounds targeting stage V gametocytes predominate in the chemical library of transmission-blocking drugs, and some of them have entered clinical trials. The targeting of Plasmodium mosquito stages has recently renewed interest in the development of innovative malaria control tools, which hold promise for the application of compounds effective at these stages. In this review, we highlight the major achievements and provide an update on the research of transmission-blocking drugs, with a particular focus on their chemical scaffolds, antiplasmodial activity, and transmission-blocking potential. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Novel Pyrazole-Containing Compounds Active against Mycobacterium tuberculosis

Author

Poce, Giovanna, primary, Consalvi, Sara, additional, Venditti, Giulia, additional, Alfonso, Salvatore, additional, Desideri, Nicoletta, additional, Fernandez-Menendez, Raquel, additional, Bates, Robert H., additional, Ballell, Lluis, additional, Barros Aguirre, David, additional, Rullas, Joaquin, additional, De Logu, Alessandro, additional, Gardner, Michelle, additional, Ioerger, Thomas R., additional, Rubin, Eric J., additional, and Biava, Mariangela, additional

Published
2019
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11. HDAC4 regulates satellite cell proliferation and differentiation by targeting P21 and Sharp1 genes

Author

Marroncelli, N., Bianchi, M., Bertin, M., Consalvi, Sara, Saccone, Valentina, De Bardi, M., Puri, P. L., Palacios, Daniela, Adamo, S., Moresi, V., Consalvi S., Saccone V. (ORCID:0000-0002-0566-6384), Palacios D. (ORCID:0000-0002-2207-2369), Marroncelli, N., Bianchi, M., Bertin, M., Consalvi, Sara, Saccone, Valentina, De Bardi, M., Puri, P. L., Palacios, Daniela, Adamo, S., Moresi, V., Consalvi S., Saccone V. (ORCID:0000-0002-0566-6384), and Palacios D. (ORCID:0000-0002-2207-2369)

Abstract

Skeletal muscle exhibits a high regenerative capacity, mainly due to the ability of satellite cells to replicate and differentiate in response to appropriate stimuli. Epigenetic control is effective at different stages of this process. It has been shown that the chromatin-remodeling factor HDAC4 is able to regulate satellite cell proliferation and commitment. However, its molecular targets are still uncovered. To explain the signaling pathways regulated by HDAC4 in satellite cells, we generated tamoxifen-inducible mice with conditional inactivation of HDAC4 in Pax7+ cells (HDAC4 KO mice). We found that the proliferation and differentiation of HDAC4 KO satellite cells were compromised, although similar amounts of satellite cells were found in mice. Moreover, we found that the inhibition of HDAC4 in satellite cells was sufficient to block the differentiation process. By RNA-sequencing analysis we identified P21 and Sharp1 as HDAC4 target genes. Reducing the expression of these target genes in HDAC4 KO satellite cells, we also defined the molecular pathways regulated by HDAC4 in the epigenetic control of satellite cell expansion and fusion.

Published
2018

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