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Prenylation Defects and Oxidative Stress Trigger the Main Consequences of Neuroinflammation Linked to Mevalonate Pathway Deregulation

Author

Listed:
  • Simona Pisanti

    (Department of Medicine, Surgery and Dentistry ′Scuola Medica Salernitana′, University of Salerno, 84081 Baronissi, Italy)

  • Erika Rimondi

    (Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy
    LTTA Centre, University of Ferrara, 44121 Ferrara, Italy)

  • Elena Pozza

    (Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy)

  • Elisabetta Melloni

    (Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy
    LTTA Centre, University of Ferrara, 44121 Ferrara, Italy)

  • Enrico Zauli

    (Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy)

  • Maurizio Bifulco

    (Department of Molecular Medicine and Medical Biotechnologies, University of Naples “Federico II”, 80131 Naples, Italy)

  • Rosanna Martinelli

    (Department of Medicine, Surgery and Dentistry ′Scuola Medica Salernitana′, University of Salerno, 84081 Baronissi, Italy)

  • Annalisa Marcuzzi

    (Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy)

Abstract

The cholesterol biosynthesis represents a crucial metabolic pathway for cellular homeostasis. The end products of this pathway are sterols, such as cholesterol, which are essential components of cell membranes, precursors of steroid hormones, bile acids, and other molecules such as ubiquinone. Furthermore, some intermediates of this metabolic system perform biological activity in specific cellular compartments, such as isoprenoid molecules that can modulate different signal proteins through the prenylation process. The defects of prenylation represent one of the main causes that promote the activation of inflammation. In particular, this mechanism, in association with oxidative stress, induces a dysfunction of the mitochondrial activity. The purpose of this review is to describe the pleiotropic role of prenylation in neuroinflammation and to highlight the consequence of the defects of prenylation.

Suggested Citation

  • Simona Pisanti & Erika Rimondi & Elena Pozza & Elisabetta Melloni & Enrico Zauli & Maurizio Bifulco & Rosanna Martinelli & Annalisa Marcuzzi, 2022. "Prenylation Defects and Oxidative Stress Trigger the Main Consequences of Neuroinflammation Linked to Mevalonate Pathway Deregulation," IJERPH, MDPI, vol. 19(15), pages 1-15, July.
    • Handle: RePEc:gam:jijerp:v:19:y:2022:i:15:p:9061-:d:871374
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    References listed on IDEAS

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    1. Rongbin Zhou & Amir S. Yazdi & Philippe Menu & Jürg Tschopp, 2011. "A role for mitochondria in NLRP3 inflammasome activation," Nature, Nature, vol. 469(7329), pages 221-225, January.
    2. Abigail Watterson & Lexus Tatge & Naureen Wajahat & Sonja L. B. Arneaud & Rene Solano Fonseca & Shaghayegh T. Beheshti & Patrick Metang & Melina Mihelakis & Kielen R. Zuurbier & Chase D. Corley & Ishm, 2022. "Intracellular lipid surveillance by small G protein geranylgeranylation," Nature, Nature, vol. 605(7911), pages 736-740, May.
    3. Rongbin Zhou & Amir S. Yazdi & Philippe Menu & Jürg Tschopp, 2011. "Erratum: A role for mitochondria in NLRP3 inflammasome activation," Nature, Nature, vol. 475(7354), pages 122-122, July.
    4. Jing Chen & Xiaochen Zhang & Liping Li & Xianqiang Ma & Chunxiao Yang & Zhaodi Liu & Chenyang Li & Maria J Fernandez-Cabezudo & Basel K al-Ramadi & Chuan Wu & Weishan Huang & Yong Zhang & Yonghui Zhan, 2021. "Farnesyl pyrophosphate is a new danger signal inducing acute cell death," PLOS Biology, Public Library of Science, vol. 19(4), pages 1-25, April.
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