Frontiers in bioscience (Landmark edition)最新文献

{"title":"Chick Embryo Chorioallantoic Membrane (CAM) Model for Cancer Studies and Drug Evaluation.","authors":"Yuzhe Wang, Wenyu Xue, Margarita Pustovalova, Denis V Kuzmin, Sergey Leonov","doi":"10.31083/FBL37456","DOIUrl":"https://doi.org/10.31083/FBL37456","url":null,"abstract":"<p><p>The chick embryo chorioallantoic membrane (CAM) model is gaining increasing attention from cancer researchers worldwide. Its affordability, short experimental duration, robustness, and ease of tumor xenograft visualization make it a valuable tool in cancer research. This review explores recent advancements and potential applications of the avian CAM model, including the following: (1) studying tumor growth and metastasis, (2) investigating mechanisms of tumor chemoresistance, (3) optimizing drug delivery methods, (4) improving bioimaging techniques, (5) evaluating immuno-oncology drug efficacy, (6) examining tumor-extracellular matrix interactions, (7) analyzing tumor angiogenesis, and (8) exploring the roles of microRNAs in cancer. Additionally, we compare the <i>in ovo</i> CAM model with other <i>in vivo</i> animal models and <i>in vitro</i> cell culture systems. Positioned between <i>in vitro</i> and <i>in vivo</i> models in terms of cost-effectiveness and accuracy in cancer recapitulation, the CAM model enhances both preclinical and translational research. Its expanding use in cancer studies and therapy development is expected to continue growing.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"37456"},"PeriodicalIF":3.3,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Melanoma Treatment with Salvianolic Acid A.","authors":"Chan-Yen Kuo","doi":"10.31083/FBL36577","DOIUrl":"https://doi.org/10.31083/FBL36577","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"36577"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acquired Piezo2 Channelopathy is One Principal Gateway to Pathophysiology.","authors":"Balázs Sonkodi","doi":"10.31083/FBL33389","DOIUrl":"https://doi.org/10.31083/FBL33389","url":null,"abstract":"<p><p>The Piezo2 transmembrane proteins were identified by Ardem Patapoutian and his team. They also found that Piezo2 is the principal mechanosensory ion channel responsible for proprioception. Even before the Nobel Prize was awarded to him, it was proposed that these Piezo2 channels could sustain acquired microdamage at the proprioceptive somatosensory terminals under allostatic stress. Moreover, the principality of Piezo2 is suggested to extend beyond its physiological function, highlighting its relevance in the context of microdamage as well. Hence, acquired Piezo2 channelopathy is proposed to constitute one principal gateway to pathophysiology underpinned by proton affinity, energy metabolism and a proprioceptive pathway switch. The differentiating incomparable hallmark of Piezo2 is theorized to be a low-frequency semiconductor Schottky barrier diode-like feature that provides proton handling for quantum tunnelling and ultrafast long-range signalling to the hippocampus. Accordingly, even the proposed acquired Piezo2 channelopathy is also enigmatic by causing the impairment of this Piezo2-initiated ultrafast proton-based long-range signalling and proper synchronization to the hippocampus. The revealing of this protonic word and the ultrafast long-range signalling within the nervous system and its microdamage brings an entirely new perspective in medicine with the interpretation of the quad-phasic non-contact injury model. This is why this Piezo2 microdamage has been coined as the primary damage or the root cause of ageing. Paired-associative electromagnetic stimulation appears to be a promising treatment method and heart rate variability detection could be used for diagnosing autonomic nervous system disbalance as one symptom of this proposed Piezo2 channelopathy.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"33389"},"PeriodicalIF":3.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plant H₂S and Transcription Factors (TFs) Interactions: Unexplored Area.","authors":"Francisco J Corpas","doi":"10.31083/FBL27736","DOIUrl":"https://doi.org/10.31083/FBL27736","url":null,"abstract":"<p><p>Plant hydrogen sulfide (H₂S) metabolism has garnered noteworthy attention due to its role in regulating many plant processes. The primary mechanism by which H₂S exerts its signaling functions is through its reversible interaction with thiol groups on cysteine residues in proteins and peptides. This thiol-based oxidative post-translational modification (oxiPTM) is known as persulfidation. Transcription factors (TFs) are key proteins that control gene expression by interacting with distinguishing DNA sequences and other regulatory proteins. Their function is essential to almost all aspects of cellular biology, including development, differentiation, and responses to environmental biotic and abiotic cues. The persulfidation of TFs has emerged as an additional regulatory mechanism, linking H₂S signaling with gene regulation. Although the available information on the crosstalk between the regulatory mechanisms of H₂S metabolism and TF activity remains limited, existing data suggest that this connection influences not only H₂S metabolism itself but also other metabolic pathways involved in various physiological and stress responses. This review provides an updated overview of an emerging research area, focusing on the mutual regulation between specific TFs and H₂S metabolism, particularly in response to adverse environmental conditions.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"27736"},"PeriodicalIF":3.3,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation Into the Pathogenesis of Type 2 Cardiorenal Syndrome via the ROS-TRPM2 Signaling Axis.","authors":"Yanxia Li, Fengrong Wang","doi":"10.31083/FBL27094","DOIUrl":"https://doi.org/10.31083/FBL27094","url":null,"abstract":"<p><strong>Background: </strong>Type 2 cardiorenal syndrome (CRS) is a complex disease characterized by the interplay between the heart and kidneys. The pathophysiology of type 2 CRS involves multiple molecular signaling pathways. Transient receptor potential melastatin 2 (TRPM2) is a reactive oxygen species (ROS)-sensitive and non-selective calcium-permeable cation channel, which plays a regulatory role in intracellular Ca²⁺ homeostasis. Thus, this study aimed to explore the biological functions and mechanisms of the ROS-TRPM2 signaling axis in type 2 CRS.</p><p><strong>Methods: </strong>Type 2 CRS model rats (a rat model of type 2 CRS induced through left anterior descending coronary artery ligation combined with 5/6 total nephrectomy) and lipopolysaccharide (LPS)-induced CRS cell lines, human kidney-2 (HK-2), were transfected with small interfering RNA (siRNA) to knock down <i>TRPM2</i> or a calcium ion channel activator Yoda1 to evaluate the involvement of the ROS-TRPM2 signaling axis on type 2 CRS. Changes in kidney tissue morphology were observed using H&E staining; cell viability and apoptosis were monitored using CCK-8, Annexin V-FITC/PI, and TUNEL kits, alongside quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, ELISA, and immunofluorescence assays to confirm the interaction between ROS, TRPM2, and Ca²⁺.</p><p><strong>Results: </strong>TRPM2 is highly expressed in HK-2 cells after LPS stimulation and renal tissues of type 2 CRS rats. Intervention via TRPM2 improves injured cell viability, mitigates apoptosis, inhibits the inflammatory cytokines interleukin 10 (IL-10) and tumor necrosis factor-α (TNF-α), as well as indices of oxidative stress-malondialdehyde (MDA) and ROS-promotes total antioxidant capacity (T-AOC) expression, and alleviates pathological changes in CRS; Yoda1 promoted a contrasting effect to the biological effect induced by TRPM2 deletion.</p><p><strong>Conclusions: </strong>TRPM2 is abnormally highly expressed in damaged kidneys during the pathogenesis of type 2 CRS. Silencing TRPM2 can inhibit inflammatory and oxidative stress responses, reduce cell apoptosis, promote survival, and alleviate pathological loss; this may be related to the inhibition of Ca²⁺ influx. This suggests that the ROS-TRPM2 signaling pathway is significant for CRS development, and TRPM2 may be an effective therapeutic target for type 2 CRS.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"27094"},"PeriodicalIF":3.3,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms and Therapeutic Targeting of Heat Shock Proteins (HSPs) in Cardiovascular Disorders.","authors":"Jyoti Upadhyay, Mukesh Nandave, Kamal Y Thajudeen, Summya Rashid, Mohd Nazam Ansari","doi":"10.31083/FBL27324","DOIUrl":"https://doi.org/10.31083/FBL27324","url":null,"abstract":"<p><p>Identifying novel biomarkers is a reliable approach to predict and diagnose human diseases as well as manage individual responses to therapeutic drugs. Heat shock proteins (HSPs) are molecular chaperones that play a major role in maintaining protein stability and folding. Many studies suggested their association with multiple types of diseases. HSPs from different categories play different roles; therefore, it is important to identify HSPs and their function to understand their biological functions clearly. This comprehensive review was performed to evaluate the role of HSPs as predictive biomarkers in cardiovascular diseases. The original publications related to HSPs from 2010 to 2024 were identified by using the keywords \"heat-shock proteins\", \"HSP in cardiovascular disorders\" and \"HSP in atherosclerosis\". The regulatory pathways involved in HSPs' functioning are the important points of discussion in this review. HSPs play a critical role in key cellular processes, including apoptosis regulation, protein folding, immune responses, genomic stability, and DNA repair. Aberrant expression of HSPs causes dysregulation of these pathways resulting in the development and progression of diseases. A comprehensive understanding of HSPs in cardiovascular diseases and their associated regulatory pathways can have significant implications for disease intervention, diagnosis, and prognosis. In this review paper, we have highlighted the importance of HSPs as versatile biomarkers and their importance as targets for the therapeutic management of cardiovascular diseases.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"27324"},"PeriodicalIF":3.3,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut Barrier, Microbial Metabolites, and Immune Homeostasis in Autoimmune Hepatitis: From Molecular Mechanisms to Strategies.","authors":"Xintong Zhang, Linyan Wan, Yujiao Zheng, Yaowei Ai","doi":"10.31083/FBL27747","DOIUrl":"https://doi.org/10.31083/FBL27747","url":null,"abstract":"<p><p>Autoimmune hepatitis (AIH) is a chronic immune-mediated inflammatory liver disease characterized by recurring immune-triggered hepatic injury. While scientists have yet to fully elucidate the precise triggers of AIH, contemporary research indicates that both gut microbiota and their metabolic products significantly influence AIH progression. These factors contribute to multiple mechanisms, including compromised intestinal barrier function, altered microbial and metabolite trafficking, and disrupted immune balance, leading to inflammatory responses. This review begins by exploring the intestinal microbial populations and their byproducts linked to AIH. It highlights how disrupted gut flora compromises intestinal immune defenses, enables bacterial migration from the gut to hepatic tissue, and induces liver inflammatory responses. Research validates that metabolic products from microbes, such as short-chain fatty acids (SCFAs), bile acids (BAs), and specific amino acids (glutamine, cysteine, tryptophan, and branched-chain variants, among others), interact with immune cell populations. These interactions, coupled with immune cell modifications, contribute to AIH progression. Our review identifies promising treatment strategies, including the use of probiotic supplementation, engineered prebiotic compounds, microbiota transfer procedures, and specific medications targeting gut microorganisms and their byproducts. These approaches could potentially reduce immune-triggered hepatic damage, offering potential new avenues for AIH management.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"27747"},"PeriodicalIF":3.3,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Lysophosphatidic Acid in Neurological Diseases: From Pathophysiology to Therapeutic Implications.","authors":"Simona Dedoni, Valeria Avdoshina, Maria C Olianas, Pierluigi Onali","doi":"10.31083/FBL28245","DOIUrl":"https://doi.org/10.31083/FBL28245","url":null,"abstract":"<p><p>Lysophosphatidic acid (LPA), a bioactive lipid molecule, has been identified as a critical regulator of several cellular processes in the central nervous system, with significant impacts on neuronal function, synaptic plasticity, and neuroinflammatory responses. While Alzheimer's disease, Multiple Sclerosis, and Parkinson's disease have garnered considerable attention due to their incidence and socioeconomic significance, many additional neurological illnesses remain unclear in terms of underlying pathophysiology and prospective treatment targets. This review synthesizes evidence linking LPA's function in neurological diseases such as traumatic brain injury, spinal cord injury, cerebellar ataxia, cerebral ischemia, seizures, Huntington's disease, amyotrophic lateral sclerosis, Hutchinson-Gilford progeria syndrome, autism, migraine, and human immunodeficiency virus (HIV)-associated complications Despite recent advances, the specific mechanisms underlying LPA's actions in various neurological disorders remain unknown, and further research is needed to understand the distinct roles of LPA across multiple disease conditions, as well as to investigate the therapeutic potential of targeting LPA receptors in these pathologies. The purpose of this review is to highlight the multiple functions of LPA in the aforementioned neurological diseases, which frequently share the same poor prognosis due to a scarcity of truly effective therapies, while also evaluating the role of LPA, its receptors, and signaling as promising actors for the development of alternative therapeutic strategies to those proposed today.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"28245"},"PeriodicalIF":3.3,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FCGR1A Alleviates Ischemic Stroke-induced Injury by Promoting Anti-Inflammatory Microglial Polarization via the AMPK-mTOR Signaling Pathway.","authors":"Meng Liu, Xuhui Fan, Dongya Chen, Huibin Yao, Zhihui Huang, Heng Li, Qing Zhang, Yuqi Wang, Haihan Song, Yufeng Yan","doi":"10.31083/FBL26614","DOIUrl":"https://doi.org/10.31083/FBL26614","url":null,"abstract":"<p><strong>Background: </strong>Ischemic stroke triggers inflammatory responses that lead to neuronal damage, with microglial polarization significantly influencing post-stroke inflammation. This study explores the role of Fc gamma receptor Ia (<i>FCGR1A</i>) in microglial polarization and its regulatory mechanisms in ischemic stroke.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) associated with ischemic stroke were identified using the GSE58294 dataset. Hub genes were found by analyzing protein-protein interaction (PPI) networks. BV2 microglia were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemic conditions <i>in vitro</i>, and <i>FCGR1A</i> and inflammatory marker levels were assessed. Besides, BV2 cells were stimulated with lipopolysaccharide (LPS) and interferon-gamma (IFN-γ) to induce M1 polarization, and the effects of <i>FCGR1A</i> overexpression and knockdown on cytokine production and microglial polarization were evaluated. The function of the AMP-activated protein kinase (AMPK)-mTOR pathway in regulating microglial polarization was further investigated using the mTOR inhibitor rapamycin (RAP).</p><p><strong>Results: </strong>From the 327 DEGs identified, <i>FCGR1A</i> was chosen as a hub gene. OGD/R treatment of BV2 cells produced a time-dependent rise in FCGR1A, induction of brown adipocytes 1 (Iba1), and interleukin 6 (IL-6) expression, indicating enhanced inflammation. <i>FCGR1A</i> overexpression induced a proinflammatory response and promoted M1 polarization, whereas <i>FCGR1A</i> knockdown reduced inflammation and shifted toward an anti-inflammatory M2 phenotype. Inhibition of the mTOR pathway using RAP, combined with <i>FCGR1A</i> knockdown, significantly enhanced AMPK activation and promoted a shift toward an anti-inflammatory M2 phenotype.</p><p><strong>Conclusion: </strong><i>FCGR1A</i> modulates microglial polarization by affecting the AMPK-mTOR signaling pathway in ischemic conditions. Targeting <i>FCGR1A</i> and related pathways could offer new therapeutic strategies to lessen inflammation and facilitate the healing process after an ischemic stroke.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"26614"},"PeriodicalIF":3.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Critical Role and Therapeutic Potential of the CXCR Family in Skin Diseases.","authors":"Jin Xu, Chaoyi Wang, Yundong Xu, Bingchen Li, Jianzhou Ye","doi":"10.31083/FBL26759","DOIUrl":"https://doi.org/10.31083/FBL26759","url":null,"abstract":"<p><p>The C-X-C chemokine receptors (CXCR) chemokine receptor family, consisting of seven primary members (CXCR1-CXCR7), is crucial in regulating immune cell recruitment, angiogenesis, cellular proliferation, and maintaining skin homeostasis and immune functions. This review evaluates the expression and roles of CXCR receptors across a range of skin cells, including keratinocytes, fibroblasts, endothelial cells, melanocytes, and various immune cells such as T cells, dendritic cells, and macrophages. Aberrations in CXCR signaling have been associated with a variety of skin disorders, such as psoriasis, atopic dermatitis, acne, and skin cancers. Despite significant advancements in the field, several critical questions persist. These include the differential effects of CXCR signaling in distinct skin pathologies and the intricate interactions between CXCR receptors and their ligands within diverse skin microenvironments. Moreover, the therapeutic targeting of the CXCR family remains unresolved, necessitating further research into its long-term efficacy and possible adverse effects. Future investigations should prioritize these critical issues to develop more effective therapeutic strategies for managing skin diseases, ultimately improving patient outcomes.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 5","pages":"26759"},"PeriodicalIF":3.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}