UNASSIGNED: Of the seventy million people who suffer from epilepsy, 40 percent of them become resistant to more than one antiepileptic medication and have a higher chance of death. While the classical definition of epilepsy was due to the imbalance between excitatory glutamatergic and inhibitory γ-aminobutyric acid (GABA)-ergic signalling, substantial evidence implicates muscarinic receptors in the regulation of neural excitability.
UNASSIGNED: Cannabinoids have shown to reduce seizure activity and neuronal excitability in several epileptic models through the activation of muscarinic receptors with drugs which modulate their activity. Cannabinoids also have been effective in reducing antiepileptic activity in pharmaco-resistant individuals; however, the mechanism of its effects in temporal lobe epilepsy is not clear.
UNASSIGNED: This review seeks to elucidate the relationship between muscarinic and cannabinoid receptors in epilepsy and neural excitability.

UNASSIGNED: The interaction between muscle and bone is shown to be clinically important but the underlying mechanisms are largely unknown. The canonical Wnt/β-catenin signaling pathway is reported to be involved in muscle-bone crosstalk, but its detailed function remains unclear. This systematic review aims to investigate and elucidate the role of the Wnt/β-catenin signaling pathways in muscle-bone crosstalk.
UNASSIGNED: We conducted a literature search on the Web of Science, PubMed, EBSCO and Embase with keywords \"Wnt*\", \"bone*\" and \"muscle*\". A systematic review was completed according to the guideline of preferred reporting items of systematic reviews and meta-analyses (PRISMA). Data synthesis included species (human, animal or cell type used), treatments involved, outcome measures and key findings with respect to Wnts.
UNASSIGNED: Seventeen papers were published from 2007 to 2021 and were extracted from a total of 1529 search results in the databases of Web of Science (468 papers), PubMed (457 papers), EBSCO (371) and Embase (233). 12 Wnt family members were investigated in the papers, including Wnt1, Wnt2, Wnt2b, Wnt3a, Wnt4, Wnt5a, Wnt8a, Wnt8b, Wnt9a, Wnt10a, Wnt10b and Wnt16. Many studies showed that muscles were able to increase or decrease osteogenesis of bone, while bone increased myogenesis of muscle through Wnt/β-catenin signaling pathways. Wnt3a, Wnt4 and Wnt10b were shown to play important roles in the crosstalk between muscle and bone.
UNASSIGNED: Wnt3a, Wnt4 and Wnt10b are found to play important mediatory roles in muscle-bone crosstalk. The role of Wnt4 was mostly found to regulate muscle from the bone side. Whilst the role of Wnt10b during muscle ageing was proposed, current evidence is insufficient to clarify the specific role of Wnt/β-catenin signaling in the interplay between sarcopenia and osteoporosis. More future studies are required to investigate the exact regulatory roles of Wnts in muscle-bone crosstalk in musculoskeletal disease models such as sarcopenia and osteoporosis.
UNASSIGNED: The systematic review provides an extensive overview to reveal the roles of Wnt/β-catenin signaling pathways in muscle-bone crosstalk. These results provide novel research directions to further understand the underlying mechanism of sarcopenia, osteoporosis, and their crosstalk, finally helping the future development of new therapeutic interventions.

The role of the plant innate immune system in the defense and symbiosis processes becomes integral in a complex network of interactions between plants and fungi. An understanding of the molecular characterization of the plant innate immune system is crucial because it constitutes plants\' self-defense shield against harmful fungi, while creating mutualistic relationships with beneficial fungi. Due to the plant-induced awareness and their complexity of interaction with fungi, sufficient assessment of the participation of the plant innate immune system in ecological balance, agriculture, and maintenance of an infinite ecosystem is mandatory. Given the current global challenge, such as the surge of plant-infectious diseases, and pursuit of sustainable forms of agriculture; it is imperative to understand the molecular language of communication between plants and fungi. That knowledge can be practically used in diverse areas, e.g., in agriculture, new tactics may be sought after to try new methods that boost crop receptiveness against fungal pathogens and reduce the dependence on chemical management. Also, it could boost sustainable agricultural practices via enhancing mycorrhizal interactions that promote nutrient absorption and optimum cropping with limited exposure of environmental contamination. Moreover, this review offers insights that go beyond agriculture and can be manipulated to boost plant conservation, environmental restoration, and quality understanding of host-pathogen interactions. Consequently, this specific review paper has offered a comprehensive view of the complex plant innate immune-based responses with fungi and the mechanisms in which they interact.

Pulmonary fibrosis (PF) is a progressive interstitial inflammatory disease with a high mortality rate. Patients with PF commonly experience a chronic dry cough and progressive dyspnoea for years without effective mitigation. The pathogenesis of PF is believed to be associated with dysfunctional macrophage polarization, fibroblast proliferation, and the loss of epithelial cells. Thus, it is of great importance and necessity to explore the interactions among macrophages, fibroblasts, and alveolar epithelial cells in lung fibrosis, as well as in the pro-fibrotic microenvironment. In this review, we discuss the latest studies that have investigated macrophage polarization and activation of non-immune cells in the context of PF pathogenesis and progression. Next, we discuss how profibrotic cellular crosstalk is promoted in the PF microenvironment by multiple cytokines, chemokines, and signalling pathways. And finally, we discuss the potential mechanisms of fibrogenesis development and efficient therapeutic strategies for the disease. Herein, we provide a comprehensive summary of the vital role of macrophage polarization in PF and its profibrotic crosstalk with fibroblasts and alveolar epithelial cells and suggest potential treatment strategies to target their cellular communication in the microenvironment.

Liver fibrosis due to viral or metabolic chronic liver diseases is a major challenge of global health. It is a critical pre‑stage condition of severe hepatopathy, characterized by excessive accumulation of extracellular matrix components and ongoing chronic inflammation. To date, early prevention of liver fibrosis remains challenging. As the most abundant non‑parenchymal hepatic cell population, liver sinusoidal endothelial cells (LSECs) are stabilizers that maintain the intrahepatic environment. Notably, LSECs dysfunction appears to be implicated in the progression of liver fibrosis via numerous mechanisms. Following sustained liver injury, they lose their fenestrae (cytoplasmic pores) and change their crosstalk with other cellular interactions in the hepatic blood environment. LSEC‑targeted therapy has shown promising effects on fibrosis resolution, opening up new opportunities for anti‑fibrotic therapy. In light of this, the present study summarized changes in LSECs during liver fibrosis and their interactions with hepatic milieu, as well as possible therapeutic approaches that specially target LSECs.

Recent scientific reports have revealed a close association between ferroptosis and the occurrence and development of osteoarthritis (OA). Nevertheless, the precise mechanisms by which ferroptosis influences OA and how to hobble OA progression by inhibiting chondrocyte ferroptosis have not yet been fully elucidated. This study aims to conduct a comprehensive systematic review (SR) to address these gaps.
Following the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020, we conducted a comprehensive search of the Embase, Ovid, ProQuest, PubMed, Scopus, the Cochrane Library, and Web of Science databases to identify relevant studies that investigate the association between ferroptosis and chondrocytes in OA. Our search included studies published from the inception of these databases until January 31st, 2023. Only studies that met the predetermined quality criteria were included in this SR.
In this comprehensive SR, a total of 21 studies that met the specified criteria were considered suitable and included in the current updated synthesis. The mechanisms underlying chondrocyte ferroptosis and its association with OA progression involve various biological phenomena, including mitochondrial dysfunction, dysregulated iron metabolism, oxidative stress, and crucial signaling pathways.
Ferroptosis in chondrocytes has opened an entirely new chapter for the investigation of OA, and targeted regulation of it is springing up as an attractive and promising therapeutic tactic for OA.
https://inplasy.com/inplasy-2023-3-0044/, identifier INPLASY202330044.

This review provides insight into the complex network of signaling pathways and mechanisms involved in stroke pathophysiology. It summarizes the historical progress of stroke-related signaling pathways, identifying potential interactions between them and emphasizing that stroke is a complex network disease. Of particular interest are the Hippo signaling pathway and ferroptosis signaling pathway, which remain understudied areas of research, and are therefore a focus of the review. The involvement of multiple signaling pathways, including Sonic Hedgehog (SHH), nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE), hypoxia-inducible factor-1α (HIF-1α), PI3K/AKT, JAK/STAT, and AMPK in pathophysiological mechanisms such as oxidative stress and apoptosis, highlights the complexity of stroke. The review also delves into the details of traditional Chinese medicine (TCM) therapies such as Rehmanniae and Astragalus, providing an analysis of the recent status of western medicine in the treatment of stroke and the advantages and disadvantages of TCM and western medicine in stroke treatment. The review proposes that since stroke is a network disease, TCM has the potential and advantages of a multi-target and multi-pathway mechanism of action in the treatment of stroke. Therefore, it is suggested that future research should explore more treasures of TCM and develop new therapies from the perspective of stroke as a network disease.

Osteosarcopenia is a burgeoning geriatric syndrome and a familiar disease among older individuals. It is characterized by reduced skeletal muscle mass and bone mineral density due to osteoporosis and sarcopenia. Its clinical manifestations include reduced physical performance and individuals becoming prone to falls during the aging process resulting in fractures and hospitalization, which seriously affects the quality of life of patients and increases the risk of death. Due to the aging social structure of the global population, the morbidity of osteosarcopenia is expected to continue to increase. Both muscle and bone belong to the motor system and originate from the mesoderm; therefore, sarcopenia and osteoporosis also share similar pathogenical factors, which influence and regulate each other. Studying the pathogenesis and treatment of osteosarcopenia is of great significance to improve the quality of life of patients. Therefore, the present study reviewed the research progress on sarcopenia and osteoporosis in osteosarcopenia from the standpoints of its definition, epidemiology, clinical manifestations and diagnosis, prevention and treatment.

Bullous pemphigoid (BP) is an autoimmune blistering disease that primarily affects elderly individuals. The presentation of BP is heterogeneous, typically manifesting as microscopic subepidermal separation with a mixed inflammatory infiltrate. The mechanism of pemphigoid development is unclear. B cells play a major role in pathogenic autoantibody production, and T cells, type II inflammatory cytokines, eosinophils, mast cells, neutrophils, and keratinocytes are also implicated in the pathogenesis of BP. Here, we review the roles of and crosstalk between innate and adaptive immune cells in BP.

Activation of CD4 T cells by B cells has been extensively studied, but B cell-regulated priming, proliferation, and survival of CD8 T cells remains controversial. B cells express high levels of MHC class I molecules and can potentially act as antigen-presenting cells (APCs) for CD8 T cells. Several in vivo studies in mice and humans demonstrate the role of B cells as modulators of CD8 T cell function in the context of viral infections, autoimmune diseases, cancer and allograft rejection. In addition, B-cell depletion therapies can lead to impaired CD8 T-cell responses. In this review, we attempt to answer 2 important questions: 1. the role of B cell antigen presentation and cytokine production in the regulation of CD8 T cell survival and cell fate determination, and 2. The role of B cells in the formation and maintenance of CD8 T cell memory.