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<p>Larval cestodiases remain difficult to treat, highlighting the need for novel therapeutic targets. The mevalonate pathway, essential for isoprenoid biosynthesis and cellular homeostasis, represents a promising target in cestodes. Previous studies demonstrated that simvastatin impairs the viability and motility of <i>Mesocestoides corti</i> tetrathyridia <i>in vitro</i>. Here, we investigated the proteomic response of <i>M. corti</i> larvae to simvastatin exposure (60.29 and 100&#xa0;µM) using DIA-based proteomics. A total of 3,378 proteins were identified, with 19 showing differential abundance across treatments. Proteomic and Gene Ontology enrichment analyses revealed dose-dependent alterations associated mainly with structural organization, metabolism, intracellular transport, and stress-related processes. Although no clear proteomic signature of cell death was detected, simvastatin induced adaptive responses consistent with compensatory remodeling in response to pharmacological stress. These findings support the biological relevance of the mevalonate pathway in cestode survival and reinforce HMG-CoA reductase as a potential target for drug repurposing strategies against larval cestodiases.</p> Graphical Abstract <p></p>

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Molecular mechanisms of simvastatin response in Mesocestoides corti: a proteomic approach to drug repurposing for larval cestodiases

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Marina Monteiro Guedes,
  • Jeferson Camargo de Lima,
  • Jéssica Andrade Paes,
  • Leo Kei Iwai,
  • Karina Mariante Monteiro,
  • Arnaldo Zaha,
  • Henrique Bunselmeyer Ferreira

摘要

Larval cestodiases remain difficult to treat, highlighting the need for novel therapeutic targets. The mevalonate pathway, essential for isoprenoid biosynthesis and cellular homeostasis, represents a promising target in cestodes. Previous studies demonstrated that simvastatin impairs the viability and motility of Mesocestoides corti tetrathyridia in vitro. Here, we investigated the proteomic response of M. corti larvae to simvastatin exposure (60.29 and 100 µM) using DIA-based proteomics. A total of 3,378 proteins were identified, with 19 showing differential abundance across treatments. Proteomic and Gene Ontology enrichment analyses revealed dose-dependent alterations associated mainly with structural organization, metabolism, intracellular transport, and stress-related processes. Although no clear proteomic signature of cell death was detected, simvastatin induced adaptive responses consistent with compensatory remodeling in response to pharmacological stress. These findings support the biological relevance of the mevalonate pathway in cestode survival and reinforce HMG-CoA reductase as a potential target for drug repurposing strategies against larval cestodiases.

Graphical Abstract