Cofilin‐1 participates in the hyperfunction of myeloid dendritic cells in patients with severe aplastic anaemia

Sun, Yingying; Zhang, Yu; Yu, Hong; Wang, Huaquan; Shao, Zhang; Liu, Chunyan

doi:10.1111/jcmm.17359

Cited by 4 publications

(2 citation statements)

References 29 publications

(66 reference statements)

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“…siRNA-induced inhibition of cofilin-1 expression can reduce phagocytosis and CD86 expression in DCs, and downregulate CD4 + and CD8 + T lymphocyte stimulation by MDC. 65 This is distinct from previous research, and further study and analysis are required.…”

Section: Increased Phagocytosis Of Myeloid Dendritic Cells In Aa Pati...mentioning

confidence: 71%

Advances in understanding the role of dendritic cells in aplastic anaemia

Gao

Zhang

2023

Scand J Immunol

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Aplastic anaemia (AA) is an autoimmune disease characterized by haematopoietic failure in the bone marrow. Abnormal activation and hyperfunction of T lymphocytes are believed to cause bone marrow damage, which plays a major role in AA pathogenesis. Dendritic cells (DCs) play a vital role in the immune system by processing antigens for presentation to T cells and regulating their differentiation and function. DC dysfunction may cause abnormal T‐cell activation. Recent studies have associated the occurrence and development of AA with DC function. In this review, we have discussed the role of DCs in AA pathogenesis and their potential as putative therapeutic targets for AA.

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Section: Increased Phagocytosis Of Myeloid Dendritic Cells In Aa Pati...mentioning

confidence: 71%

Advances in understanding the role of dendritic cells in aplastic anaemia

Gao

Zhang

2023

Scand J Immunol

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“…These inflammatory signals contribute to the recruitment of more immune cells and exacerbate neuronal damage [97,98]. It also impacts actin dynamics in immune cells, contributing to processes such as immune synapse formation and phagocytosis [99]. Cofilin activation in astrocytes can also contribute to neuroinflammation by promoting the release of pro-inflammatory cytokines and chemokines [90].…”

Section: Neuroinflammation In Stroke Its Implications and Cofilin As ...mentioning

confidence: 99%

The Multifaceted Role of Cofilin in Neurodegeneration and Stroke: Insights into Pathogenesis and Targeting as a Therapy

Shehjar,

Almarghalani,

Mahajan

et al. 2024

Cells

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This comprehensive review explores the complex role of cofilin, an actin-binding protein, across various neurodegenerative diseases (Alzheimer’s, Parkinson’s, schizophrenia, amyotrophic lateral sclerosis (ALS), Huntington’s) and stroke. Cofilin is an essential protein in cytoskeletal dynamics, and any dysregulation could lead to potentially serious complications. Cofilin’s involvement is underscored by its impact on pathological hallmarks like Aβ plaques and α-synuclein aggregates, triggering synaptic dysfunction, dendritic spine loss, and impaired neuronal plasticity, leading to cognitive decline. In Parkinson’s disease, cofilin collaborates with α-synuclein, exacerbating neurotoxicity and impairing mitochondrial and axonal function. ALS and frontotemporal dementia showcase cofilin’s association with genetic factors like C9ORF72, affecting actin dynamics and contributing to neurotoxicity. Huntington’s disease brings cofilin into focus by impairing microglial migration and influencing synaptic plasticity through AMPA receptor regulation. Alzheimer’s, Parkinson’s, and schizophrenia exhibit 14-3-3 proteins in cofilin dysregulation as a shared pathological mechanism. In the case of stroke, cofilin takes center stage, mediating neurotoxicity and neuronal cell death. Notably, there is a potential overlap in the pathologies and involvement of cofilin in various diseases. In this context, referencing cofilin dysfunction could provide valuable insights into the common pathologies associated with the aforementioned conditions. Moreover, this review explores promising therapeutic interventions, including cofilin inhibitors and gene therapy, demonstrating efficacy in preclinical models. Challenges in inhibitor development, brain delivery, tissue/cell specificity, and long-term safety are acknowledged, emphasizing the need for precision drug therapy. The call to action involves collaborative research, biomarker identification, and advancing translational efforts. Cofilin emerges as a pivotal player, offering potential as a therapeutic target. However, unraveling its complexities requires concerted multidisciplinary efforts for nuanced and effective interventions across the intricate landscape of neurodegenerative diseases and stroke, presenting a hopeful avenue for improved patient care.

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