Actin polymerization and depolymerization in developing vertebrates

Bai, Yang; Zhao, Feng; Wu, Tingting; Chen, Fangchun; Pang, Xiaoxiao

doi:10.3389/fphys.2023.1213668

Cited by 3 publications

(1 citation statement)

References 325 publications

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“…This results in a higher turnover of actin filaments within the cytoskeleton. The increased depolymerization leads to a surplus of free globular (G)-actin monomers within the cellular pool, making them available for new filament assembly [76]. The combined actions of cofilin result in a shift in the dynamic equilibrium of actin filaments.…”

Section: Cytoskeletal Disruptionmentioning

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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Section: Cytoskeletal Disruptionmentioning

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

View full text Add to dashboard Cite

show abstract

Piezo1 – Serine/threonine-protein phosphatase 2A – Cofilin1 biochemical mechanotransduction axis controls F-actin dynamics and cell migration

Morena,

Argentati,

Caponi

et al. 2024

Heliyon

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Natural killer cell migration in HIV-infected individuals is inhibited by impairment of HIF-1α-mediated glycolysis

Yu,

Zhou,

Lei

et al. 2024

Preprint

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Natural killer (NK) cells serve as the first line of defense of the immune system and play a crucial role in fighting against HIV infection. The effective function of NK cells is closely related to their migration ability, but the status of NK cell migration in HIV-infected individuals and the regulation mechanism for NK cell migration remains unknown. Here, we found that NK cell migration was significantly impaired in HIV-infected individuals, lower in immune non-responders (INRs) compared with immune responders (IRs), and positively correlated with CD4+T cell counts. Further investigations showed that the decreased NK cell migration in HIV infection was caused by the impairment of glycolysis. Mechanistically, we found that NK cell migration was regulated by HIF-1α pathway, and inhibitory receptor TIGIT restrained HIF-1α expression by inhibiting PI3K/AKT/mTORC1 or ERK signaling pathway, consequently weakening the glycolysis of NK cells in HIV-infected individuals, and ultimately leading to down-regulation of migration. Collectively, we uncovered a mechanism of reduced NK cell migration in HIV infection and provided a new insight for immunotherapy in HIV infection.In BriefThe effective function of NK cells is closely related to its migration ability. The authors show that impaired NK cell migration in HIV-infected individuals is caused by TIGIT inhibiting HIF-1α-mediated glycolysis via PI3K/AKT/mTORC1 or ERK pathway.

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Actin polymerization and depolymerization in developing vertebrates

Cited by 3 publications

References 325 publications

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

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

Piezo1 – Serine/threonine-protein phosphatase 2A – Cofilin1 biochemical mechanotransduction axis controls F-actin dynamics and cell migration

Natural killer cell migration in HIV-infected individuals is inhibited by impairment of HIF-1α-mediated glycolysis

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