Biomolecules最新文献_第3页

Proteomics Approaches for Discovering Novel Protein Biomarkers in Inflammatory Bowel Disease-Related Cancer. 在炎性肠病相关癌症中发现新的蛋白质生物标志物的蛋白质组学方法。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-17 DOI: 10.3390/biom15091328

Tommaso Saccon, Matilde Bergamo, Cinzia Franchin

{"title":"Proteomics Approaches for Discovering Novel Protein Biomarkers in Inflammatory Bowel Disease-Related Cancer.","authors":"Tommaso Saccon, Matilde Bergamo, Cinzia Franchin","doi":"10.3390/biom15091328","DOIUrl":"10.3390/biom15091328","url":null,"abstract":"Inflammatory bowel disease (IBD) is an autoimmune condition with an increasing incidence worldwide, which manifests in two pathological forms: Crohn's disease (CD) or ulcerative colitis (UC). Both cause chronic inflammation of the digestive tract, although they can present different locations and with different symptoms. To date, the pathogenesis of IBD remains unclear. One of the major complications of these diseases is colorectal cancer. Several studies have reported a correlation between chronic intestinal inflammation and an increased risk of malignancy. Persistent inflammation damages the intestinal mucosa and epithelial wall, altering gut permeability and the local microenvironment. Moreover, the heightened activity of the immune system leads to an increased production of reactive oxygen and nitrogen species (ROS and RNS), increasing the risk of DNA mutation and cell transformation. In addition, some current therapies used to treat IBD and induce remission may contribute to carcinogenesis or impair immune surveillance due to their immunosuppressive activity. The management of cancer risk for IBD patients remains a challenge, and existing screening methods are often invasive (endoscopies, biopsies), resulting in low patient compliance. To address this unmet clinical need, researchers have started using proteomics to identify novel biomarkers that could predict cancer risk in IBD patients in a non-invasive manner. This review aims to examine the current state of knowledge regarding the correlation between IBD and cancer, with a special focus on the biomarkers discovered through proteomic approaches, and their potential application in routine clinical screening. In our view, proteomics represents a powerful and rapidly evolving strategy for biomarker discovery, with the potential to complement or even replace invasive procedures. Its future clinical impact will rely on translating current research advances into robust and accessible diagnostic tools.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bile Acids Are Potential Negative Allosteric Modulators of M1 Muscarinic Receptors. 胆汁酸是M1毒蕈碱受体的潜在负变构调节剂。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-17 DOI: 10.3390/biom15091326

Wenbo Yu, Alexander D MacKerell, David J Weber, Jean-Pierre Raufman

{"title":"Bile Acids Are Potential Negative Allosteric Modulators of M1 Muscarinic Receptors.","authors":"Wenbo Yu, Alexander D MacKerell, David J Weber, Jean-Pierre Raufman","doi":"10.3390/biom15091326","DOIUrl":"10.3390/biom15091326","url":null,"abstract":"The proposed physiological roles of bile acids have expanded beyond the digestion of fats to encompass cell signaling via the activation of a variety of nuclear and plasma membrane receptors in multiple organ systems. The current in silico study was inspired by previous observations from our group and others that bile acids interact functionally with cardiac, pulmonary, and gastrointestinal muscarinic receptors and more recent work demonstrating allosteric binding of cholesterol, the parent molecule for bile acid synthesis, to M1 muscarinic receptors (M1R). Here, we computationally tested the hypothesis that bile acids can allosterically bind to M1R and thereby modulate receptor activation. Utilizing de novo site identification by the ligand competitive saturation (SILCS) method, putative novel allosteric binding sites of bile acid targeting M1R were identified. Molecular dynamics simulations were used to uncover the molecular details of the activation mechanism of M1R due to agonist binding along with allosteric modulation of bile acids on M1R activation. Allosteric binding of bile acids and their glycine and taurine conjugates to M1R negatively impacts the activation process, findings consistent with recent reports that M1R expression and activation inhibit colon cancer cell proliferation. Thus, bile acids may augment colon cancer risk by inhibiting the tumor suppressor actions of M1R. When validated experimentally, these findings are anticipated to shed light on our understanding of how bile acids in the membrane microenvironment can allosterically modulate the function of M1R and possibly other G protein-coupled receptors.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pinocembrin Downregulates Vascular Smooth Muscle Cells Proliferation and Migration Leading to Attenuate Neointima Formation in Balloon-Injured Rats. 匹诺曹下调血管平滑肌细胞增殖和迁移导致球囊损伤大鼠新生内膜形成减弱。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-17 DOI: 10.3390/biom15091325

Hyeonhwa Kim, Jihye Jung, Young-Bob Yu, Dong-Hyun Choi, Leejin Lim, Heesang Song

{"title":"Pinocembrin Downregulates Vascular Smooth Muscle Cells Proliferation and Migration Leading to Attenuate Neointima Formation in Balloon-Injured Rats.","authors":"Hyeonhwa Kim, Jihye Jung, Young-Bob Yu, Dong-Hyun Choi, Leejin Lim, Heesang Song","doi":"10.3390/biom15091325","DOIUrl":"10.3390/biom15091325","url":null,"abstract":"The abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are a primary cause of cardiovascular diseases such as atherosclerosis and restenosis after angioplasty. Pinocembrin (5,7-dihydroxyflavanone, PCB), a natural flavonoid compound found abundantly in propolis, has been reported to have antibacterial, anti-inflammatory, antioxidant, and anticancer effects, and cardiac function improvement in ischemic heart disease. In this study, the protective effects of PCB against the migration and proliferation of VSMCs were investigated. MTT and BrdU assays were performed to estimate the cytotoxicity and cell proliferative activity of PCB, respectively. Rat aortic VSMC migrations and neointima formation were evaluated using wound healing, boyden chamber assays, and in balloon-injured (BI) rat, respectively. PCB suppressed the phosphorylated levels of p38 in PDGF-BB-induced VSMCs followed by reducing the expression of MMP2 and 9. PCB downregulated the expression levels of cell cycle regulatory proteins such as PCNA, CDK2, CDK4, and Cyclin D1. Furthermore, the phosphorylated levels of FAK at Y397 and Y925 sites and the expression levels of FAK-related proteins such as Integrin β1, Paxillin, Talin, and Vinculin were significantly reduced by PCB in PDGF-BB-induced VSMCs. The neointima formation was markedly decreased by PCB administration in the carotid artery of a balloon-injured rat. In conclusion, PCB inhibits the proliferation and migration of VSMCs by stimulation of PDGF-BB through the regulation of the p38 and FAK signaling pathway. Therefore, PCB may be a promising therapeutic candidate for preventing and treating cardiovascular diseases such as atherosclerosis and restenosis.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pyruvate Kinase M2 Links Metabolism and Epigenetics: A New Target for Liver Disease Treatment. 丙酮酸激酶M2连接代谢和表观遗传学：肝病治疗的新靶点。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-17 DOI: 10.3390/biom15091327

Xiaoya Zhang, Danmei Zhang, Jin Guo, Chunxia Shi, Zuojiong Gong

引用次数: 0

AARS1 and AARS2: From Protein Synthesis to Lactylation-Driven Oncogenesis. AARS1和AARS2：从蛋白质合成到乳酸化驱动的肿瘤发生。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-16 DOI: 10.3390/biom15091323

Lingyue Gao, Jihua Guo, Rong Jia

{"title":"AARS1 and AARS2: From Protein Synthesis to Lactylation-Driven Oncogenesis.","authors":"Lingyue Gao, Jihua Guo, Rong Jia","doi":"10.3390/biom15091323","DOIUrl":"10.3390/biom15091323","url":null,"abstract":"Aminoacyl-tRNA synthetases (AARSs), traditionally recognized for their essential role in protein synthesis, are now emerging as critical players in cancer pathogenesis through translation-independent functions. Lactate-derived lactylation, a post-translational modification, plays an increasingly important role in tumorigenesis in the context of high levels of lactate in tumor cells due to the Warburg effect. Current research has highlighted AARS1/2 as lactate sensors and lactyltransferases that catalyze global lysine lactylation in cancer cells and promote cancer proliferation, providing a new perspective for cancer therapy. This review synthesizes the canonical and non-canonical functions of AARS1/2, with a particular focus on their lactylation-related mechanisms; details how lactylation acts as a mechanistic bridge linking AARS1/2 to diverse oncogenic signaling pathways, thereby promoting cancer hallmarks such as metabolic reprogramming, uncontrolled proliferation, immune escape, and therapy resistance; and proposes strategies to target AARS1/2 or modulate relative lactylation, offering a potential avenue to translate these insights into effective cancer therapies.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LRRK2-Mediated Neuroinflammation-Induced Neuronal Dysfunctions in a Parkinson's and Alzheimer's Disease Cellular Model. lrrk2介导的帕金森病和阿尔茨海默病细胞模型中神经炎症诱导的神经元功能障碍

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-16 DOI: 10.3390/biom15091322

Veronica Mutti, Giulia Carini, Moira Marizzoni, Alice Filippini, Federica Bono, Chiara Fiorentini, Samantha Saleri, Floriana De Cillis, Annamaria Cattaneo, Massimo Gennarelli, Paolo Martini, Isabella Russo

{"title":"LRRK2-Mediated Neuroinflammation-Induced Neuronal Dysfunctions in a Parkinson's and Alzheimer's Disease Cellular Model.","authors":"Veronica Mutti, Giulia Carini, Moira Marizzoni, Alice Filippini, Federica Bono, Chiara Fiorentini, Samantha Saleri, Floriana De Cillis, Annamaria Cattaneo, Massimo Gennarelli, Paolo Martini, Isabella Russo","doi":"10.3390/biom15091322","DOIUrl":"10.3390/biom15091322","url":null,"abstract":"Chronic neuroinflammation plays a crucial role in the progression of neurodegenerative diseases (NDs), including Parkinson's disease (PD) and Alzheimer's disease (AD). Leucine-Rich Repeat Kinase 2 (LRRK2), a gene linked to familial and sporadic PD, has been positively associated with neuroinflammation in both in vitro and in vivo systems. These observations suggest that LRRK2 might actively contribute to neuronal damage and degeneration in NDs. Based on these premises, we explored the impact of LRRK2-mediated neuroinflammation on neurons in a PD- and AD-related context. We set up a cellular model composed of human induced pluripotent stem cell (hiPSC)-derived neurons (dopaminergic for PD and cholinergic for AD) exposed to inflamed glial medium [α-synuclein pre-formed fibrils (α-syn pffs) for PD and amyloid-β (Aβ)1-42 fibrils for AD] for several days. To dissect the effect of neuroinflammation, and specifically, the role of LRRK2, on neuronal functions, we first performed transcriptome analysis, and then, we validated the results at functional levels. Interestingly, we found that LRRK2-dependent neuroinflammation contributes to neuronal dysfunctions and death in both ND contexts and that LRRK2 kinase inhibition prevents these detrimental effects. Overall, our results suggest that lowering neuroinflammation through LRRK2 pharmacological inhibition might limit the progression of NDs and thus be neuroprotective.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EET-Based Therapeutics Mitigate Sorafenib-Associated Glomerular Cell Damage. 基于eet的治疗减轻索拉非尼相关的肾小球细胞损伤。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-16 DOI: 10.3390/biom15091324

Abhishek Mishra, Marcus de Bourg, Rawand S Mohamed, Md Abdul Hye Khan, Tsigereda Weldemichael, Donald J Johann, Samaneh Goorani, Shobanbabu Bommagani, Darin E Jones, Anders Vik, John D Imig

{"title":"EET-Based Therapeutics Mitigate Sorafenib-Associated Glomerular Cell Damage.","authors":"Abhishek Mishra, Marcus de Bourg, Rawand S Mohamed, Md Abdul Hye Khan, Tsigereda Weldemichael, Donald J Johann, Samaneh Goorani, Shobanbabu Bommagani, Darin E Jones, Anders Vik, John D Imig","doi":"10.3390/biom15091324","DOIUrl":"10.3390/biom15091324","url":null,"abstract":"Background: This study investigates how sorafenib induces toxicity in glomerular cells and examines the protective role of 8,9-epoxyeicosatrienoic acid (8,9-EET) analogs in reducing this kidney damage.Methods: Human renal mesangial cells (HRMCs) and podocytes were treated with no treatment, sorafenib alone, or sorafenib combined with 8,9-EET analogs. Cell viability and apoptosis were measured in both cell types.Results: Sorafenib (1-10 µM) lowered cell viability and increased caspase 3/7 activity in a dose-dependent way in HRMCs and podocytes. Five of twenty 8,9-EET analogs significantly enhanced cell survival and decreased apoptosis. RNA sequencing showed that sorafenib altered 1244 genes, including those involved in cell cycle and the Raf/MEK/ERK pathway. The 8,9-EET analog MDB-52a raised ANGPTL4 levels, linked to metabolism and vascular health, and reduced ACTA2, which could activate protective pathways. Nephroseq data correlated these gene changes with glomerulosclerosis.Conclusions: MDB-52 appears to counteract gene disruptions and protect against sorafenib-induced kidney damage. Overall, 8,9-EET analogs targeting glomerular cells could be potential therapeutic agents to lessen sorafenib-related nephrotoxicity.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activin A Secreted by Cancer-Associated Fibroblasts Reduces the Sensitivity of Breast Cancer Cells to Ixazomib via Inhibition of Proteasome Activity. 癌症相关成纤维细胞分泌的激活素A通过抑制蛋白酶体活性降低乳腺癌细胞对伊沙唑米的敏感性

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-15 DOI: 10.3390/biom15091318

Shuaiming Geng, Siyao Liu, He Liu, Siao Wang, Yichen Niu, Jing Gao, Yong Meng, Mingqing Gao

{"title":"Activin A Secreted by Cancer-Associated Fibroblasts Reduces the Sensitivity of Breast Cancer Cells to Ixazomib via Inhibition of Proteasome Activity.","authors":"Shuaiming Geng, Siyao Liu, He Liu, Siao Wang, Yichen Niu, Jing Gao, Yong Meng, Mingqing Gao","doi":"10.3390/biom15091318","DOIUrl":"10.3390/biom15091318","url":null,"abstract":"Breast cancer (BC) remains a leading cause of cancer-related mortality among women globally, and the role of cancer-associated fibroblasts (CAFs) in promoting BC progression is well established. Ixazomib, a proteasome inhibitor approved for the treatment of multiple myeloma, has demonstrated therapeutic potential in BC in preclinical trials. However, whether its efficacy is influenced by the tumor microenvironment, particularly CAFs, remains unclear. This study aims to investigate the role of CAFs with high expression of Activin A (encoded by INHBA) in modulating the sensitivity of BC cells to ixazomib. We demonstrate that ixazomib exhibited significant cytotoxicity in BC cells, but high-INHBA CAFs compromise ixazomib cytotoxicity through ERK-mediated proteasome suppression, reversible by Activin A antagonism. Additionally, the overexpression of INHBA in fibroblasts reduces the efficacy of ixazomib in xenograft models. Clinical data analysis revealed that high INHBA expression is associated with poor prognosis in BC patients and reduced immune cell infiltration. These findings suggest that targeting INHBA in CAFs could enhance the therapeutic efficacy of ixazomib in BC, particularly in patients with low INHBA expression. This study provides novel insights into the role of CAFs in drug resistance and identifies INHBA as a potential therapeutic target.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Population-Level Dynamics and Community-Mediated Resistance to Antimicrobial Peptides. 种群水平动态和群落介导的抗菌肽耐药性。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-15 DOI: 10.3390/biom15091319

Theresia Mekdessi, Aracely Devora, Sattar Taheri-Araghi

{"title":"Population-Level Dynamics and Community-Mediated Resistance to Antimicrobial Peptides.","authors":"Theresia Mekdessi, Aracely Devora, Sattar Taheri-Araghi","doi":"10.3390/biom15091319","DOIUrl":"10.3390/biom15091319","url":null,"abstract":"Antimicrobial peptides (AMPs) are crucial components of innate immunity and promising leads for new anti-infective therapies, prized for their broad-spectrum activity and membrane-disruptive mechanisms. However, traditional models of antimicrobial action and resistance often focus on single-cell responses or genetically encoded resistance, overlooking the complex collective behaviors of bacteria at the population level. A growing body of evidence indicates that bacterial communities can profoundly influence AMP efficacy through emergent, community-level resistance mechanisms. In this review, we examine how population-level dynamics and interactions enable bacteria to withstand AMPs beyond what is predicted by cell-autonomous models. We first describe the mechanisms of peptide sequestration by bacterial debris, dead cells, outer membrane vesicles, and biofilm matrix polymers, which diminish the concentration of active peptide available to kill neighboring cells. We then analyze how population-level traits-including inoculum effects, phenotypic heterogeneity, and persister subpopulations-shape survival outcomes and promote regrowth after treatment. Cooperative processes such as protease secretion further enhance communal defenses by coordinating or amplifying protective responses. Beyond cataloging these mechanisms, we highlight recent advances in microfluidic tools, single-cell imaging, and biophysical modeling that reveal the spatial and temporal dynamics of AMP action in structured populations. Collectively, these insights show how bacterial communities absorb, neutralize, or delay AMP activity without genetic resistance, with important implications for therapeutic design and the evaluation of AMP efficacy.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Approach to a Child with Hypophosphatemia. 低磷血症儿童的治疗方法。

IF 4.8 2区生物学

Biomolecules Pub Date : 2025-09-15 DOI: 10.3390/biom15091321

Agnieszka Antonowicz, Patryk Lipiński, Michał Popow, Piotr Skrzypczyk

{"title":"Approach to a Child with Hypophosphatemia.","authors":"Agnieszka Antonowicz, Patryk Lipiński, Michał Popow, Piotr Skrzypczyk","doi":"10.3390/biom15091321","DOIUrl":"10.3390/biom15091321","url":null,"abstract":"Hypophosphatemia is a rare ion disorder in children, but it carries the risk of serious clinical sequelae in tissues and organs with high energy requirements, such as bone tissue. This article discusses the metabolism of phosphate in the body, the clinical manifestations of hypophosphatemia, and the diagnostic tests necessary in patients with this disorder. Extra-renal causes are analyzed, and renal forms of hypophosphatemia are discussed in detail. Renal hypophosphatemia, depending on the mechanism, is divided into PTH-dependent (e.g., primary hyperparathyroidism), FGF23-dependent (e.g., X-linked hypophosphatemia), and intrinsic renal hypophosphatemia (e.g., Fanconi syndrome). The treatment of hypophosphatemia involves compensating for phosphate deficiency, often simultaneously with the supply of an active form of vitamin D. Always seek causal treatment, such as parathyroidectomy in primary hyperparathyroidism. In the FGF-23-dependent forms of X-linked hypophosphatemia and tumor-induced osteomalacia, burosumab has proven to be an effective and safe drug. Conclusions: a child with hypophosphatemia requires a multidisciplinary approach and determination of the mechanism of phosphate deficiency in the body.","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"15 9","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0