Inflammation is highlighted as a key pathology in central nervous system (CNS) diseases, whose overactivation can release cytokines or other inflammatory mediators, leading to local neuronal damage and function impairment. Microglia and astrocytes are resident immune cells contributing to neuroinflammation by producing cytokines or growth factors, mediating phagocytosis, and modulating the interaction of resident and peripheral immune responses in CNS.
Neuroinflammation is multifactorial that is intimately linked to the temporal and spatial control of gene expression mediated by noncoding RNAs (ncRNAs). ncRNAs are mainly divided into short (microRNAs), long (lncRNAs), and circular RNAs (circRNAs). They mediate neuroinflammation through multidimensional mechanisms, including transcriptional, post-transcriptional, and post-translational pathways involved in different CNS pathologies. ncRNAs also form a sophisticated network by interacting with other molecules to regulate the expression or activation of downstream pathways, such as NF-?B and JAK-STAT pathways which are highly correlated with a pro-inflammatory response. Neuroinflammation-associated ncRNAs may act as therapeutic targets and prognostic factors in neurological diseases. Thus, understanding the molecular mechanisms in the context of ncRNA-based multi-signaling pathways and seeking novel drug targets and candidates in neuroinflammation will aid in the knowledge of the initiation and progression of CNS diseases and help establish therapeutic strategies targeting neuroinflammation.
This Research Topic explores the ncRNA-associated function and molecular mechanism in the immune-inflammatory responses of CNS diseases, especially ischemic stroke, intracerebral hemorrhage, neurodegenerative disorders, traumatic and spinal cord brain injury, etc. Meanwhile, this Research Topic focuses on the latest progress in the potential of innovative ncRNA-oriented pharmacological interventions and the development of drugs targeting ncRNAs and neuroinflammation, which will help achieve a beneficial impact on the pathogenesis and therapeutic discovery in CNS diseases.
This Research Topic aims to publish high-quality articles within the ncRNA-bridged neuroinflammation area to provide emerging experimental discoveries, novel insights, and conceptual advancements for CNS diseases and move the neurotherapeutic field forward. We encourage the submission of Original Research, Review, Systematic Review, Mini Review, Perspective, Case Report, and Data Report articles covering, but not limited to, the following subtopics:
1) Functions and signaling pathways of novel ncRNAs (microRNAs, lncRNAs, circRNAs, etc.) in inflammatory reactions of CNS diseases;
2) Mechanisms of new epigenetic modifications on ncRNAs involved in neuroinflammation;
3) Discovery of ncRNA-based drug molecules and therapies for the treatment of CNS diseases.
Inflammation is highlighted as a key pathology in central nervous system (CNS) diseases, whose overactivation can release cytokines or other inflammatory mediators, leading to local neuronal damage and function impairment. Microglia and astrocytes are resident immune cells contributing to neuroinflammation by producing cytokines or growth factors, mediating phagocytosis, and modulating the interaction of resident and peripheral immune responses in CNS.
Neuroinflammation is multifactorial that is intimately linked to the temporal and spatial control of gene expression mediated by noncoding RNAs (ncRNAs). ncRNAs are mainly divided into short (microRNAs), long (lncRNAs), and circular RNAs (circRNAs). They mediate neuroinflammation through multidimensional mechanisms, including transcriptional, post-transcriptional, and post-translational pathways involved in different CNS pathologies. ncRNAs also form a sophisticated network by interacting with other molecules to regulate the expression or activation of downstream pathways, such as NF-?B and JAK-STAT pathways which are highly correlated with a pro-inflammatory response. Neuroinflammation-associated ncRNAs may act as therapeutic targets and prognostic factors in neurological diseases. Thus, understanding the molecular mechanisms in the context of ncRNA-based multi-signaling pathways and seeking novel drug targets and candidates in neuroinflammation will aid in the knowledge of the initiation and progression of CNS diseases and help establish therapeutic strategies targeting neuroinflammation.
This Research Topic explores the ncRNA-associated function and molecular mechanism in the immune-inflammatory responses of CNS diseases, especially ischemic stroke, intracerebral hemorrhage, neurodegenerative disorders, traumatic and spinal cord brain injury, etc. Meanwhile, this Research Topic focuses on the latest progress in the potential of innovative ncRNA-oriented pharmacological interventions and the development of drugs targeting ncRNAs and neuroinflammation, which will help achieve a beneficial impact on the pathogenesis and therapeutic discovery in CNS diseases.
This Research Topic aims to publish high-quality articles within the ncRNA-bridged neuroinflammation area to provide emerging experimental discoveries, novel insights, and conceptual advancements for CNS diseases and move the neurotherapeutic field forward. We encourage the submission of Original Research, Review, Systematic Review, Mini Review, Perspective, Case Report, and Data Report articles covering, but not limited to, the following subtopics:
1) Functions and signaling pathways of novel ncRNAs (microRNAs, lncRNAs, circRNAs, etc.) in inflammatory reactions of CNS diseases;
2) Mechanisms of new epigenetic modifications on ncRNAs involved in neuroinflammation;
3) Discovery of ncRNA-based drug molecules and therapies for the treatment of CNS diseases.
