Biomolecules & Therapeutics最新文献_第5页

Ferroptosis-Driven Senescence Loop as a Central Amplifier of Osteoarthritis Progression. 嗜铁细胞驱动的衰老环是骨关节炎进展的中心放大器。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2026.010

Rajib Hossain, Hyun Jae Lee, Md Solayman Hossain, Jiwon Jeong, Choong Jae Lee, Sun-Chul Hwang

{"title":"Ferroptosis-Driven Senescence Loop as a Central Amplifier of Osteoarthritis Progression.","authors":"Rajib Hossain, Hyun Jae Lee, Md Solayman Hossain, Jiwon Jeong, Choong Jae Lee, Sun-Chul Hwang","doi":"10.4062/biomolther.2026.010","DOIUrl":"10.4062/biomolther.2026.010","url":null,"abstract":"Osteoarthritis (OA) is a prevalent, chronic joint disorder characterized by cartilage degradation, synovial inflammation, and extracellular matrix (ECM) remodeling, yet disease-modifying therapies remain elusive. Emerging evidence implicates ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, and cellular senescence, characterized by growth arrest and a senescence-associated secretory phenotype (SASP), as central contributors to OA pathogenesis. Ferroptotic chondrocytes release reactive lipid species and damage-associated molecular patterns (DAMPs) that induce paracrine senescence in neighboring cells, while senescent cells amplify oxidative stress and ferroptotic susceptibility, forming a self-perpetuating feed-forward loop that accelerates tissue degeneration. Histological, molecular, and in vivo studies demonstrate iron accumulation, lipid peroxidation, glutathione peroxidase 4 (GPX4) depletion, and SASP factor secretion in human OA cartilage, synovium, and animal models, linking these processes to ECM breakdown and joint inflammation. Targeted interventions, alone or in combination, can disrupt this pathological loop, preserve chondrocyte viability, reduce SASP-mediated inflammation, and mitigate cartilage damage. Integration of biomarker-guided patient stratification, advanced imaging, and spatial transcriptomic profiling may enable precision-targeted, disease-modifying therapies. Therefore, elucidating the crosstalk between ferroptosis and senescence offers a conceptual and translational framework for shifting OA management from symptomatic relief toward preservation of joint integrity and long-term disease modification.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"506-518"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Adenosine A₁ and A_2A Receptors in Sleep Disorders: Mechanisms and Therapeutic Implications. 睡眠障碍中的腺苷A1和A2A受体：机制和治疗意义。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2026.070

Hye Jin Jee, Cherin Youn, Haeun Lee, Yi-Sook Jung

{"title":"Adenosine A1 and A2A Receptors in Sleep Disorders: Mechanisms and Therapeutic Implications.","authors":"Hye Jin Jee, Cherin Youn, Haeun Lee, Yi-Sook Jung","doi":"10.4062/biomolther.2026.070","DOIUrl":"10.4062/biomolther.2026.070","url":null,"abstract":"Sleep-wake regulation is controlled by circadian and homeostatic processes, with adenosine acting as a key molecular mediator of homeostatic sleep pressure. Extracellular adenosine accumulates during wakefulness as a result of neuronal energy metabolism, particularly in the basal forebrain, and declines during recovery sleep, thereby reflecting the physiological need for sleep. The sleep-promoting effects of adenosine are mediated primarily by two G protein-coupled receptor subtypes, the adenosine A1 receptor and the adenosine A2A receptor. The adenosine A1 receptor, coupled to inhibitory Gi/o proteins and widely expressed in the cortex, hippocampus, thalamus, and basal forebrain, suppresses wake-promoting neuronal activity and facilitates slow-wave activity during non-rapid eye movement sleep. In contrast, the adenosine A2A receptor, coupled to stimulatory Golf proteins and enriched in the striatum and nucleus accumbens, promotes sleep by activating neurons in the preoptic hypothalamus and engaging the indirect basal ganglia pathway. Despite these well-established roles, the contributions of dysregulation of the adenosine A1 receptor and the adenosine A2A receptor to specific sleep disorders remain incompletely understood. This review examines how signaling of the adenosine A1 receptor and the adenosine A2A receptor is altered in insomnia, obstructive sleep apnea, narcolepsy, and restless legs syndrome, and evaluates the therapeutic potential of receptor-selective strategies for adenosine receptor-targeted treatment.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"461-470"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Structure-Activity Relationships and Ligand-Dependent Arrestin Bias in μ-Opioid Receptor-Mediated ERK Activation. μ-阿片受体介导的ERK激活的结构-活性关系和配体依赖的抑制因子偏倚。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2025.255

Lei Huang, Mengling Wang, Dooti Kundu, Suresh Paudel, Lulu Peng, Xinru Xian, Choon-Gon Jang, Kyeong-Man Kim

{"title":"Structure-Activity Relationships and Ligand-Dependent Arrestin Bias in μ-Opioid Receptor-Mediated ERK Activation.","authors":"Lei Huang, Mengling Wang, Dooti Kundu, Suresh Paudel, Lulu Peng, Xinru Xian, Choon-Gon Jang, Kyeong-Man Kim","doi":"10.4062/biomolther.2025.255","DOIUrl":"10.4062/biomolther.2025.255","url":null,"abstract":"This study elucidated the structure-activity relationships (SAR) of three distinct opioid ligand series at the µ-opioid receptor (µ-OR) and investigated the ligand-dependent role of arrestin in downstream signaling. Radioligand binding assays across 13 compounds revealed that high-affinity µ-OR binding is not restricted to a single chemical scaffold. For fentanyl analogs, SAR analysis identified four key structural determinants: the N-phenethyl group (R1) is essential for µ-OR binding, the piperidine 4-position (R2) is sterically constrained and tolerates only small substituents such as carbomethoxy, the acyl side chain (R3) tolerates diverse chemical modifications including alkyl, alkoxy, and heteroaryl groups without substantial loss of affinity, and para-substitution on the phenethyl ring (R4) with electron-withdrawing groups like fluorine is well-tolerated. Analysis of non-fentanyl scaffolds (2-Methyl AP-237, W-15, and brorphine) demonstrated that specific side-chain functionalization, rather than core scaffold architecture, primarily determines binding potency. Comparison of classical opioids further revealed that structural flexibility, exemplified by methadone, can confer superior binding affinity compared to the rigid morphine scaffold. Consistent with this structural diversity, the contribution of arrestins to ERK activation varied substantially across compounds, suggesting that µ-OR-biased signaling is not dictated exclusively by intrinsic receptor properties but emerges from the interplay between receptor conformation and ligand-specific structural features. Collectively, our results provide a molecular framework for understanding opioid pharmacology with important implications for rational drug design aimed at minimizing adverse effects while maintaining analgesic efficacy.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"556-564"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Current and Emerging Therapies Targeting the IL-23/IL-17 Axis in Psoriasis. 靶向IL-23/IL-17轴治疗银屑病的现有和新兴疗法。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2026.019

Sang-Jun Han, Go-Yeon Jung, Gyeong-Cheon Lee, Dae-Hee Ki, Byung-Seok Kim

{"title":"Current and Emerging Therapies Targeting the IL-23/IL-17 Axis in Psoriasis.","authors":"Sang-Jun Han, Go-Yeon Jung, Gyeong-Cheon Lee, Dae-Hee Ki, Byung-Seok Kim","doi":"10.4062/biomolther.2026.019","DOIUrl":"10.4062/biomolther.2026.019","url":null,"abstract":"Over the past two decades, experimental and clinical evidence has established the interleukin-23 (IL-23)/interleukin-17 (IL-17) axis as a key mediator of psoriatic inflammation. IL-23, primarily derived from activated dendritic cells, supports the survival and pathogenic function of type 17 immune cells, which subsequently release IL-17A, IL-17F, and IL-22 to promote keratinocyte activation and recruit inflammatory leukocytes. These mechanistic insights have directly translated into the development of highly effective biologic therapies targeting IL-17 or IL-23, substantially improving the management of psoriasis. Beyond injectable biologics, growing efforts to overcome limitations related to long-term adherence, cost, and accessibility have accelerated the development of non-injectable therapeutic approaches. Oral and topical small-molecule agents, including selective tyrosine kinase 2 (TYK2) inhibitors and IL-23 receptor antagonists, are now broadening the therapeutic options. At the same time, progress in molecular engineering, artificial intelligence-guided protein design, and spatial multi-omic technologies are refining therapeutic discovery and enabling more precise targeting of pathogenic immune circuits. In this review, we outline the current understanding of the IL-23/IL-17 pathway in psoriasis pathogenesis and provide a critical overview of approved and emerging therapies directed at this pathway. We also address key biological and translational challenges, including tissue-specific cytokine functions, interspecies differences, and long-term safety considerations, and discuss how these factors may inform future strategies for precision immunotherapy in psoriasis.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"519-529"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Caffeic Acid Protects Keratinocytes from PM_2.5 by Regulating ROS, Mitochondrial Integrity, and JNK Activation. 咖啡酸通过调节ROS、线粒体完整性和JNK激活来保护角质形成细胞免受PM2.5的影响。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2025.254

Herath Mudiyanselage Maheshika Madhuwanthi Senavirathna, Mei Jing Piao, Kyoung Ah Kang, Mahadurage Pasindu Laksara Madhuwantha, Jinny Park, Jin Won Hyun

{"title":"Caffeic Acid Protects Keratinocytes from PM2.5 by Regulating ROS, Mitochondrial Integrity, and JNK Activation.","authors":"Herath Mudiyanselage Maheshika Madhuwanthi Senavirathna, Mei Jing Piao, Kyoung Ah Kang, Mahadurage Pasindu Laksara Madhuwantha, Jinny Park, Jin Won Hyun","doi":"10.4062/biomolther.2025.254","DOIUrl":"10.4062/biomolther.2025.254","url":null,"abstract":"Caffeic acid (CA) is a naturally occurring phenolic compound known for its strong antioxidant and cytoprotective properties. Particulate matter (PM) with an aerodynamic diameter of 2.5 µm (PM2.5) or less is a major atmospheric pollutant that induces excessive oxidative stress and apoptosis in human skin cells, contributing to various adverse effects on the skin. In this study, we investigated the protective role of CA against PM2.5-induced cellular injury in human HaCaT keratinocytes. CA reduced PM2.5-induced reactive oxygen species (ROS) accumulation and mitigated oxidative damage, including lipid peroxidation, protein carbonyl formation, mitochondrial membrane depolarization, and intracellular calcium overload. In addition, CA attenuated PM2.5-induced apoptosis by upregulating B-cell lymphoma 2 (Bcl-2) and suppressing Bcl-2-associated X protein (Bax), caspase-3, caspase-9, and phosphorylated c-Jun N-terminal kinase (phospho-JNK). Collectively, these findings demonstrate that CA protects HaCaT keratinocytes from PM2.5-induced oxidative stress and apoptosis by regulating the Bcl-2/Bax axis and inhibiting JNK-mediated apoptotic signaling, highlighting its potential as a therapeutic candidate for preventing pollutant-induced skin damage.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"697-708"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Adipocytes as Orchestrators of Multimodal Cancer Therapy Resistance. 脂肪细胞是多模式癌症治疗耐药的协调者。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2026.036

Jinseon Park, Jaebeom Cho

{"title":"Adipocytes as Orchestrators of Multimodal Cancer Therapy Resistance.","authors":"Jinseon Park, Jaebeom Cho","doi":"10.4062/biomolther.2026.036","DOIUrl":"10.4062/biomolther.2026.036","url":null,"abstract":"The emergence of therapy resistance remains a formidable barrier to successful clinical outcomes in oncology, necessitating a deeper understanding of the tumor microenvironment (TME) as a dynamic ecosystem. Adipocytes, once viewed as passive energy reservoirs, are now recognized as active orchestrators of tumor progression and multimodal therapy resistance, particularly in adipose-rich malignancies. This review comprehensively delineates the multifaceted mechanisms through which adipocytes shield cancer cells from therapeutic insults, including chemotherapy, targeted agents, and immunotherapies. We analyze the clinical evidence positioning visceral adiposity as a critical determinant of treatment failure and explore the complex molecular interplay driven by the adipocyte-derived secretome, lipid metabolite-mediated metabolic rewiring, and the horizontal transfer of bioactive cargo via adipocyte-derived extracellular vesicles, and adipocyte-mediated remodeling of the TME. Furthermore, we highlight noncanonical roles such as direct organelle donation, lipid-mediated drug sequestration, the enhancement of DNA repair pathways, and the activation of cell adhesion-dependent survival signaling. We also synthesize recent technological advancements employed to interrogate the intricate adipocyte-cancer interaction. Finally, we discuss emerging therapeutic strategies aimed at disrupting the adipocyte-cancer axis, while critically addressing the translational limitations of these interventions in clinical settings, offering a roadmap for integrating metabolic and anti-inflammatory interventions with standard regimens to overcome adipocyte-driven resistance and advance precision oncology.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"491-505"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Proarrhythmic Risk Assessment of Sildenafil under High-Dose Misuse Conditions Using the Comprehensive In Vitro Proarrhythmia Assay (CiPA). 利用综合体外心律失常测定（CiPA）评估西地那非在大剂量滥用条件下的心律失常风险。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2025.097

Hanbi Kim, Tae Woong Na, Inkyo Jung, Minji Kang, Sujeong Park, Chan Hyeok Kwon, Kikyung Jung

{"title":"Proarrhythmic Risk Assessment of Sildenafil under High-Dose Misuse Conditions Using the Comprehensive In Vitro Proarrhythmia Assay (CiPA).","authors":"Hanbi Kim, Tae Woong Na, Inkyo Jung, Minji Kang, Sujeong Park, Chan Hyeok Kwon, Kikyung Jung","doi":"10.4062/biomolther.2025.097","DOIUrl":"10.4062/biomolther.2025.097","url":null,"abstract":"The comprehensive in vitro proarrhythmia assay (CiPA) initiative, led by the U.S. Food and Drug Administration (FDA), provides a framework for predicting drug-induced arrhythmia risk. To support domestic CiPA implementation, we evaluated the proarrhythmic risk of sildenafil, a phosphodiesterase type 5 (PDE5) inhibitor. Sildenafil has been misused recreationally, with reports of high-dose non-medical intake. To simulate misuse, in vitro assays were conducted using concentrations up to 100× the maximum therapeutic plasma concentration (Cmax). The assessment followed the three core components of the CiPA paradigm. Patch clamp assays were conducted in Human Embryonic Kidney 293 (HEK293) and Chinese hamster ovary (CHO) cells transiently expressing Nav1.5, Cav1.2, and hERG ion channels. In silico modeling was performed using the CiPAORdv1.0 model based on IC₅₀ and Hill coefficient values. Functional evaluation included multi-electrode array (MEA) recordings in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), and in vivo electrocardiography (ECG) analysis in rats was performed to observe QT interval prolongation. Sildenafil significantly inhibited hERG currents by 40.5% at 100× Cmax. In silico modeling predicted a low Torsades de Pointes (TdP) risk based on qNet biomarkers. In contrast, MEA recordings showed a concentration-dependent prolongation of corrected field potential duration (FPDc), with a significant 13.3% increase at 100× Cmax. The TdP risk estimated from MEA modeling was 64%. In vivo ECG analysis revealed significant QT prolongation at 50× Cmax. Despite low in silico TdP predictions, functional assays suggest that high concentrations of sildenafil as in misuse may pose a clinically relevant risk of QT prolongation and arrhythmia.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"578-588"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MHY5456, an FXR Agonist, Ameliorates Hepatic Steatosis and Fibrosis in a Mouse Model of MASLD. FXR激动剂MHY5456改善MASLD小鼠模型中的肝脏脂肪变性和纤维化

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2025.256

Mi-Jeong Kim, Hyejin Kang, Jian Yoo, Sugyeong Ha, Jeongwon Kim, Byeong Moo Kim, Da Eun Park, Hae Young Chung, Donghwan Kim, Hyung Ryong Moon, Ki Wung Chung

{"title":"MHY5456, an FXR Agonist, Ameliorates Hepatic Steatosis and Fibrosis in a Mouse Model of MASLD.","authors":"Mi-Jeong Kim, Hyejin Kang, Jian Yoo, Sugyeong Ha, Jeongwon Kim, Byeong Moo Kim, Da Eun Park, Hae Young Chung, Donghwan Kim, Hyung Ryong Moon, Ki Wung Chung","doi":"10.4062/biomolther.2025.256","DOIUrl":"10.4062/biomolther.2025.256","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a global health issue due to its increasing prevalence associated with lifestyle changes and its strong correlation with metabolic syndrome. Farnesoid X receptor (FXR) is a nuclear receptor that plays a pivotal role in regulating bile acid, lipid, and glucose metabolism, making it an attractive therapeutic target for liver and metabolic diseases. In this study, we investigated the effects of MHY5456, a synthetic agonist of FXR, on hepatic metabolism and fibrosis. MHY5456 enhanced the transcriptional activity of FXR in a concentration-dependent manner. Treatment of AC2F rat liver-derived cells with MHY5456 resulted in the downregulation of genes involved in lipid accumulation and an upregulation of mitochondrial-related gene expression. Additionally, MHY5456 significantly reduced oleic acid (OA)-induced lipid accumulation. To assess its anti-fibrotic potential, we tested its effects on transforming growth factor-beta (TGF-β)-induced fibrosis in LX2 human hepatic stellate cells (HSCs). MHY5456 significantly suppressed the expression of fibrosis-related genes and proteins. In vivo, administration of MHY5456 to mice fed a methionine-choline-deficient (MCD) diet alleviated hepatic fibrosis, inflammation, and lipid accumulation. These results show that FXR activation by MHY5456 modulates lipid metabolism and fibrotic pathways, suggesting its potential as a pharmacological candidate for liver and metabolic disorders, including MASLD. Further pharmacological and toxicological studies are needed to confirm its therapeutic relevance.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"652-665"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phytotherapeutic Potential of Medicinal Plants for Atopic Dermatitis: Centella asiatica, Clinacanthus nutans, Senna alata, and Coccinia grandis. 药用植物治疗特应性皮炎的潜力：积雪草、山棘草、番泻草和大球虫。

IF 4.9 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2025-04-30 DOI: 10.4062/biomolther.2025.115

Thitiluck Swangsri, Naowarat Saralamba

{"title":"Phytotherapeutic Potential of Medicinal Plants for Atopic Dermatitis: Centella asiatica, Clinacanthus nutans, Senna alata, and Coccinia grandis.","authors":"Thitiluck Swangsri, Naowarat Saralamba","doi":"10.4062/biomolther.2025.115","DOIUrl":"10.4062/biomolther.2025.115","url":null,"abstract":"Atopic dermatitis (AD) is a chronic inflammatory skin disorder with significant global health implications, particularly in low-resource settings. In many Asian countries, traditional herbal medicine remains an integral part of healthcare and presents promising alternatives for managing AD. This review examines the therapeutic potential of four ethnomedicinal plants; Centella asiatica, Clinacanthus nutans, Senna alata, and Coccinia grandis, focusing on their anti-inflammatory, antimicrobial, and antioxidant activities. Evidence from preclinical and clinical studies highlights key bioactive compounds and underlying mechanisms, demonstrating their efficacy in alleviating AD symptoms and supporting skin barrier restoration. Comparative analysis suggests complementary and potentially synergistic effects across these species, targeting multiple aspects of AD pathophysiology. However, translation into clinical practice is constrained by inconsistent formulations, limited human trials, bioavailability challenges, and regulatory variability. Future directions include the development of standardized extracts, nanotechnology-based delivery systems, integration with conventional therapies, omics-driven precision medicine, and harmonized regulatory frameworks. Collectively, these strategies outline a therapeutic development pipeline for advancing plant-based interventions for AD from traditional use to clinical application.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"530-543"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum to "Glycogen Phosphorylase Inhibitor Promotes Hair Growth via Protecting from Oxidative-Stress and Regulating Glycogen Breakdown in Human Hair follicles" [Biomol Ther 32(5), 640-646 (2024)]. “糖原磷酸化酶抑制剂通过保护氧化应激和调节人毛囊糖原分解促进头发生长”[j].中国生物医学工程学报，32(5),640-646（2024）。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2026-05-01 Epub Date: 2026-04-30 DOI: 10.4062/biomolther.2026.008

Bomi Park, Daeun Kim, Hairu Zhao, SoonRe Kim, Byung Cheol Park, Sanghwa Lee, Yurim Lee, Hee Dong Park, Dongchul Lim, Sunyoung Ryu, Jae Sung Hwang

引用次数: 0