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Type I Interferon Signalling and Ischemic Stroke: Mechanisms and Therapeutic Potentials

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Abstract

Type I interferon (IFN-I) signalling is intricately involved in the pathogenesis of multiple infectious diseases, autoimmune diseases, and neurological diseases. Acute ischemic stroke provokes overactivation of IFN-I signalling within the injured brain, particularly in microglia. Following cerebral ischemia, damage-associated molecular patterns (DAMPs) released from injured neural cells elicit marked proinflammatory episodes within minutes. Among these, self-nucleic acids, including nuclear DNA and mitochondrial DNA (mtDNA), have been recognized as a critical alarm signal to fan the flames of neuroinflammation, predominantly via inducing IFN-I signalling activation in microglia. The concept of interferon-responsive microglia (IRM), marked by upregulation of a plethora of IFN-stimulated genes, has been emergingly elucidated in ischemic mouse brains, particularly in aged ones. Among the pattern recognition receptors responsible for IFN-I induction, cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) plays integral roles in potentiating microglia-driven neuroinflammation and secondary brain injury after cerebral ischemia. Here, we aim to provide an up-to-date review on the multifaceted roles of IFN-I signalling, the detailed molecular and cellular mechanisms leading to and resulting from aberrant IFN-I signalling activation after cerebral ischemia, and the therapeutic potentials. A thorough exploration of these above points will inform our quest for IFN-based therapies as effective immunomodulatory therapeutics to complement the limited repertoire of thrombolytic agents, thereby facilitating the translation from bench to bedside.

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Funding

This review was supported by the National Natural Science Foundation of China (Grant U1904207 and 91849115 to YX) and the Nonprofit Central Research Institute Fund of Chinese Academy of Medical Sciences (Grant 2020PT31001 to YX).

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Authors and Affiliations

  1. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China

    Pan Cui, Bo Song, Zongping Xia & Yuming Xu

  2. NHC Key Laboratory of Prevention and Treatment of Cerebrovascular Diseases, Zhengzhou, Henan, China

    Pan Cui, Bo Song, Zongping Xia & Yuming Xu

  3. Clinical Systems Biology Laboratories, Translation Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, China

    Pan Cui & Zongping Xia

  4. Henan Key Laboratory of Cerebrovascular Diseases, Zhengzhou University, Zhengzhou, Henan, China

    Yuming Xu

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The central concept of this review was proposed by YX, ZX, and PC. PC and BS outlined the manuscript. PC was responsible for the comprehensive literature search for references and contributed to drafting the manuscript, creating the figures, and organizing the tables. BS was involved in the critical revision of the manuscript. YX and ZX were responsible for the final revision and overall content. The submission was approved by all authors.

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Correspondence to Zongping Xia or Yuming Xu.

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Cui, P., Song, B., Xia, Z. et al. Type I Interferon Signalling and Ischemic Stroke: Mechanisms and Therapeutic Potentials. Transl. Stroke Res. (2024). https://doi.org/10.1007/s12975-024-01236-x

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