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MINI REVIEW article

Front. Immunol.
Sec. Molecular Innate Immunity
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1375428

What could be the function of the Spinal Muscular Atrophy-causing protein SMN in macrophages?

Provisionally accepted
Ines Tapken Ines Tapken 1,2Nora T. Detering Nora T. Detering 1,2Peter Claus Peter Claus 1,2*
  • 1 Zentrum für Systemische Neurowissenschaften (ZSN), Hannover, Lower Saxony, Germany
  • 2 SMATHERIA gGmbH, Hannover, Germany

The final, formatted version of the article will be published soon.

    Spinal Muscular Atrophy (SMA), a neurodegenerative disorder, extends its impact beyond the nervous system. The central protein implicated in SMA, Survival Motor Neuron (SMN) protein, is ubiquitously expressed and functions in fundamental processes such as alternative splicing, translation, cytoskeletal dynamics and signaling. These processes are relevant for all cellular systems, including cells of the immune system such as macrophages. Macrophages are capable of modulating their splicing, cytoskeleton and expression profile in order to fulfil their role in tissue homeostasis and defense. However, less is known about impairment or dysfunction of macrophages lacking SMN and the subsequent impact on the immune system of SMA patients. We aimed to review the potential overlaps between SMN functions and macrophage mechanisms highlighting the need for future research, as well as the current state of research addressing the role of macrophages in SMA.

    Keywords: macrophage, monocyte, spinal muscular atrophy, SMA, SMN, SMN gene, neurodegeneration

    Received: 23 Jan 2024; Accepted: 06 May 2024.

    Copyright: © 2024 Tapken, Detering and Claus. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Peter Claus, Zentrum für Systemische Neurowissenschaften (ZSN), Hannover, 30559, Lower Saxony, Germany

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