Biomolecules & Therapeutics最新文献

IFI16 Enhances Chemosensitivity of Breast Cancer Cells by Inhibiting DNA Damage Response. IFI16通过抑制DNA损伤反应增强乳腺癌细胞的化疗敏感性。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-10-02 DOI: 10.4062/biomolther.2025.085

Na-Lee Ka, Ga Young Lim, Seung-Su Kim, Mi-Ock Lee

{"title":"IFI16 Enhances Chemosensitivity of Breast Cancer Cells by Inhibiting DNA Damage Response.","authors":"Na-Lee Ka, Ga Young Lim, Seung-Su Kim, Mi-Ock Lee","doi":"10.4062/biomolther.2025.085","DOIUrl":"https://doi.org/10.4062/biomolther.2025.085","url":null,"abstract":"Many chemotherapeutic agents exert their cytotoxic effects primarily by inducing DNA damage. In response to DNA damage, cells activate a signaling cascade known as DNA damage response (DDR) to repair the damage and promote cell survival. Accordingly, the capacity of the DDR in cancer cells is a critical factor that influences their sensitivity to chemotherapy. Here, we identified a role for interferon γ-inducible protein 16 (IFI16) in modulating the DDR and chemosensitivity of breast cancer cells. Depletion of IFI16 in MDA-MB-231 cells conferred resistance to the DNA-damaging agents doxorubicin and 5-fluorouracil, as evidenced by increased cell viability and reduced caspase-3 cleavage compared to control cells. Mechanistically, IFI16 interacted with the MRE11-RAD50-NBS1 complex and disrupted the interaction between NBS1 and ataxia telangiectasia mutated (ATM), a critical step for ATM activation. In vivo, xenograft tumors derived from IFI16 knockout cells exhibited diminished responses to doxorubicin treatment, characterized by decreased apoptotic cell death and reduced expression of DSB marker proteins, such as γH2AX and 53BP1. Furthermore, analysis of breast cancer patient datasets revealed that high IFI16 expression correlated with an improved pathological complete response rate following chemotherapy. Our findings suggest that IFI16 could serve as both a predictive biomarker for chemotherapy response and a potential therapeutic target for enhancing the efficacy of DNA-damaging agents.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

N-Acetyldopamine Dimer from Cicadidae Periostracum Is Enantioselectively Neuroprotective via Antioxidant Property. 蝉的n -乙酰多巴胺二聚体通过抗氧化作用对神经具有选择性保护作用。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-10-02 DOI: 10.4062/biomolther.2025.140

Punam Thapa, Shristi Khanal, Kibria Gulam, Trung Huy Ngo, Zhiying Chen, Young Jun Ok, Kyu Joon Lee, Hyukjae Choi, Joo-Won Nam, Dong-Young Choi

{"title":"N-Acetyldopamine Dimer from Cicadidae Periostracum Is Enantioselectively Neuroprotective via Antioxidant Property.","authors":"Punam Thapa, Shristi Khanal, Kibria Gulam, Trung Huy Ngo, Zhiying Chen, Young Jun Ok, Kyu Joon Lee, Hyukjae Choi, Joo-Won Nam, Dong-Young Choi","doi":"10.4062/biomolther.2025.140","DOIUrl":"https://doi.org/10.4062/biomolther.2025.140","url":null,"abstract":"N-Acetyldopamine oligomers are typically biosynthesized as racemic mixtures, yet enantiomers can differ markedly in pharmacological efficacy and safety. In this study, we isolated a pair of enantiomers of an N-acetyldopamine dimer (compound 1) from Cicadidae Periostracum, a traditional medicinal substance, and characterized their structures using mass spectrometry and 1D/2D NMR spectroscopy. The absolute configurations of the enantiomers-1a (2S,3R,1''R) and 1b (2R,3S,1''S)-were determined for the first time through a combination of electronic circular dichroism and Mosher's esterification analysis. Biological evaluation revealed striking differences in activity between the two enantiomers. Specifically, 1a exhibited significant neuroprotective effects against rotenone-induced cytotoxicity in SH-SY5Y neuroblastoma cells, while 1b was inactive. Compound 1a attenuated oxidative stress by reducing intracellular and mitochondrial reactive oxygen species and elevating glutathione levels. Mechanistically, only 1a activated nuclear factor erythroid 2-related factor 2 (Nrf2), a key regulator of antioxidant defenses. Molecular docking studies further indicated a stronger interaction of 1a with Keap1, the repressor of Nrf2, suggesting a structural basis for the enantioselective activation of the pathway. To our knowledge, this is the first report to assign the absolute configuration at C-1'' of this class of compounds and to demonstrate enantioselective neuroprotective activity mediated by the Nrf2 pathway. These findings underscore the therapeutic potential of insect-derived chiral natural products and provide a rationale for developing stereochemically defined neuroprotective agents for the treatment of neurodegenerative diseases such as Parkinson's disease.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transforming Pain Management: Suzetrigine, a Novel Non-Opioid Analgesic. 改变疼痛管理：舒三嗪，一种新型非阿片类镇痛药。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-10-01 DOI: 10.4062/biomolther.2025.046

Maha AlDoughaim, Nada AlSuhebany, Mohammed AlZahrani, Atheer AlDairem, Sahar S Alghamdi

引用次数: 0

Dietary Potassium Synergistically Enhances Anti-Obesity Efficacy of Garcinia Cambogia Complex in High-Fat Diet-Induced Obese Mice. 膳食钾协同提高藤黄果复合物对高脂肪饮食诱导的肥胖小鼠的抗肥胖功效。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-10-01 DOI: 10.4062/biomolther.2025.069

Eunji Park, Sehan Kwak, Ayoung Lim, Suji Lee, Min Seok Park, Yun Ji Lee, Sang Eun Kim, Ye Jin Cho, Pureunchowon Lee, Hee-Seung Lee, Hong-Mei Zheng, Sang Hun Lee, Soon-Sun Hong, Kyung Hee Jung

{"title":"Dietary Potassium Synergistically Enhances Anti-Obesity Efficacy of Garcinia Cambogia Complex in High-Fat Diet-Induced Obese Mice.","authors":"Eunji Park, Sehan Kwak, Ayoung Lim, Suji Lee, Min Seok Park, Yun Ji Lee, Sang Eun Kim, Ye Jin Cho, Pureunchowon Lee, Hee-Seung Lee, Hong-Mei Zheng, Sang Hun Lee, Soon-Sun Hong, Kyung Hee Jung","doi":"10.4062/biomolther.2025.069","DOIUrl":"https://doi.org/10.4062/biomolther.2025.069","url":null,"abstract":"Obesity is a global health problem associated with several metabolic disorders. Conventional dietary supplements such as Garcinia cambogia, catechin, and conjugated linoleic acid (GC complex) are widely used for weight loss but raise concerns about long-term efficacy and safety. Recent advances in nutritional research suggest that combining dietary mineral elements might enhance obesity therapeutic outcomes. The objective of this study is to investigate the potential synergistic effects of potassium in combination with GC complex in a mouse model of high-fat diet (HFD)-induced obesity. When administered daily orally for 12 weeks, the HFD+GC+Potassium group exhibited synergistically reduced adipocyte size in both white and brown adipose tissue compared to the HFD group, indicating a reduction in fat storage. In addition, HFD+GC+Potassium group exhibited a marked improvement in metabolic profiles, characterized by reduced fasting glucose and total cholesterol levels without toxicity, compared with HFD group. Histological analyses confirmed the effectiveness of the treatment, showing marked reductions in hepatic steatosis and lipid accumulation, as evidenced by H&E and Oil Red-O staining in the HFD+GC+Potassium group. Significantly, the study showed that potassium supplementation in combination with GC complex improved lipid metabolism and energy expenditure by increasing the expression of phosphorylated acetyl-CoA carboxylase 1 (p-ACC1) and carnitine palmitoyltransferase I (CPT1), while decreasing the levels of fatty acid synthase (FAS) and sterol regulatory element-binding protein 1 (SREBP1) through IGF1R/ PI3K/AKT/GSK3β axis. These findings suggest that the combination of GC complex and dietary potassium may offer a synergistic effect and a safe strategy for managing obesity by reducing fat accumulation and enhancing metabolic health.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aberrantly High Expression of Steroid Receptor Coactivator-1 Drives Lung Cancer Growth and Metastasis by Enhancing Cancer Stemness. 类固醇受体共激活因子-1的异常高表达通过增强肿瘤干性驱动肺癌生长和转移。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-10-01 DOI: 10.4062/biomolther.2025.082

Jinjin Pan, Haoran Zhou, Liang Liu, Shuo Xu, Yu Hou, Ke Cheng, Yuan Li, Chenggong Zhu, Na Wu, Chunmei Bai, Ruoqing Wang, Changhong Liu, Rui Wang, Yuhui Yuan

{"title":"Aberrantly High Expression of Steroid Receptor Coactivator-1 Drives Lung Cancer Growth and Metastasis by Enhancing Cancer Stemness.","authors":"Jinjin Pan, Haoran Zhou, Liang Liu, Shuo Xu, Yu Hou, Ke Cheng, Yuan Li, Chenggong Zhu, Na Wu, Chunmei Bai, Ruoqing Wang, Changhong Liu, Rui Wang, Yuhui Yuan","doi":"10.4062/biomolther.2025.082","DOIUrl":"https://doi.org/10.4062/biomolther.2025.082","url":null,"abstract":"Steroid receptor coactivator-1 (SRC-1) is documented in various cancers and primarily mediates tumor growth and metastasis. Nevertheless, the specific effects and underlying mechanisms of SRC-1 in lung cancer have not been fully explored. This study aims to elucidate the role of SRC-1 in lung cancer progression and its impact on cancer stemness. In this study, we found that SRC-1 was expressed higher in human lung cancer tissues compared to normal lung tissues, with a positive correlation between SRC-1 expression and rates of distant metastasis and lymph node involvement. High SRC-1 expression was correlated with a poor prognosis of lung cancer. In vitro, silencing SRC-1 in lung cancer cell lines repressed cell proliferation, invasion, migration, and enhanced the sensitivity of lung cancer cells to gefitinib. In vivo, silencing SRC-1 in lung cancer cells decreased tumor size and weight in a subcutaneous xenograft mouse model. Furthermore, SRC-1 knockdown inhibited the lung metastasis and reduced twist1 expression. Mechanistically, SRC-1 promoted sphere formation and induced increased expression of the markers of cancer stem cells in lung cancer cells. Besides, SRC-1 positively correlated with c-Myc in human lung cancer. Overexpression of SRC-1 in lung cancer cell lines up-regulated mRNA and protein expression of c-Myc, suggesting that SRC-1 may enhance lung cancer stemness via up-regulating c-Myc. This study demonstrated that aberrantly high levels of SRC-1 in lung cancer contribute to tumor growth and metastasis by enhancing cancer stemness, suggesting that targeting SRC-1 could be a novel potential therapeutic strategy in the treatment of lung cancer.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Brazilein Impedes IKK Activation by Disrupting RIPK1 Polyubiquitination, Increasing Apoptotic Susceptibility in Cells with Constitutively Active NF-κ. 巴西蛋白通过破坏RIPK1多泛素化来阻碍IKK的激活，增加NF-κ组成活性细胞的凋亡敏感性。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-19 DOI: 10.4062/biomolther.2025.099

Kyeong Ah Park, Hee Sun Byun, Jaehee Ha, Chan Sol Kim, Kyung-Cheol Sohn, Sanghee Shin, Chan-Yong Park, Yeon-Jae Cho, Ill Young Lee, Gang Min Hur

{"title":"Brazilein Impedes IKK Activation by Disrupting RIPK1 Polyubiquitination, Increasing Apoptotic Susceptibility in Cells with Constitutively Active NF-κ.","authors":"Kyeong Ah Park, Hee Sun Byun, Jaehee Ha, Chan Sol Kim, Kyung-Cheol Sohn, Sanghee Shin, Chan-Yong Park, Yeon-Jae Cho, Ill Young Lee, Gang Min Hur","doi":"10.4062/biomolther.2025.099","DOIUrl":"https://doi.org/10.4062/biomolther.2025.099","url":null,"abstract":"Ubiquitination of RIPK1 serves as a critical regulatory switch in determining the outcome of prosurvival NF-κB signaling by linking the TNFR1 signaling complex to upstream IKK activation. Therefore, identifying bioactive compounds that modulate RIPK1 ubiquitination has emerged as a promising strategy to enhance the therapeutic efficacy of TNF, particularly in cancers with constitutively active NF-κB signaling. In our previous in vitro phytochemical study, we demonstrated that brazilin, isolated from Caesalpinia sappan L., inhibits the catalytic activity of the IKK complex during TNF-mediated NF-κB activation without affecting RIPK1 ubiquitination at high concentrations (~50 μM), raising concerns about off-target effects. In this study, we now report that brazilein, an oxidized derivative of brazilin, acts as a potent inhibitor of RIPK1-dependent NF-κB activation upon TNFR1 engagement. Our findings reveal that brazilein markedly suppresses upstream IKK signaling events, including TNFR1-associated RIPK1 polyubiquitination and its interaction with IKKβ. In contrast, brazilein does not affect NIK/IKKκ-mediated non-canonical NF-κB activation induced by LIGHT, indicating its specificity for the canonical NF-κB pathway. Moreover, brazilein not only sensitizes cells to TNF-induced apoptosis but also induces apoptosis in A20-deficient and oncogenically transformed cells with constitutive NF-κB activity. Taken together, these results suggest a novel mechanism by which brazilein exerts anti-IKK activity through inhibition of RIPK1 ubiquitination, highlighting its potential as a candidate for NF-κB-targeted cancer therapy.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chitinase-3-Like Protein 1 as a Therapeutic Target for Inflammatory Diseases. 几丁质酶-3样蛋白1作为炎性疾病的治疗靶点。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-07 DOI: 10.4062/biomolther.2025.050

Sun Mi Gu, Tae Hun Kim, Jeong Ho Park, Key-Hwan Lim, Po Myoung Jun, Yong Sun Lee, Gi Ryang Kweon, Jin Tae Hong

{"title":"Chitinase-3-Like Protein 1 as a Therapeutic Target for Inflammatory Diseases.","authors":"Sun Mi Gu, Tae Hun Kim, Jeong Ho Park, Key-Hwan Lim, Po Myoung Jun, Yong Sun Lee, Gi Ryang Kweon, Jin Tae Hong","doi":"10.4062/biomolther.2025.050","DOIUrl":"10.4062/biomolther.2025.050","url":null,"abstract":"Chitinase-3-like protein 1 (CHI3L1) is a secreted glycoprotein involved in macrophage polarization, apoptosis, and inflammation, and carcinogenesis. The expression of CHI3L1 is significantly increased in various inflammatory and immunological diseases, such as rheumatoid arthritis, Alzheimer's disease, and atopic dermatitis. Several studies suggest that CHI3L1 may be a viable therapeutic target for these diseases, given its ability to release various pro-inflammatory cytokines, including interleukin (IL)-1β, IL-4, IL-6, IL-13, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). Therefore, CHI3L1 likely plays a role in the development of a broad spectrum of inflammatory diseases. However, the precise pathophysiological and pharmacological mechanisms by which CHI3L1 contributes to these diseases remain to be fully elucidated. This review synthesizes recent findings on the functional roles of CHI3L1 across diverse inflammatory conditions, highlighting its involvement in critical signaling pathways. Moreover, preclinical research underscores the therapeutic potential of CHI3L1 inhibition. Thus, targeted CHI3L1 interventions represent a compelling therapeutic strategy warranting further clinical exploration and validation.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"747-757"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793393","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

Inhibitory Effect of a Novel Non-Steroidal AMPamide on Inflammation and Sebogenesis by Suppressing TLR4 and TLR6-Mediated Signaling Pathway. 新型非甾体AMPamide通过抑制TLR4和tlr6介导的信号通路对炎症和皮脂生成的抑制作用

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-06 DOI: 10.4062/biomolther.2025.072

Myo Hyeon Park, Yu Ra Jung, Eun Bi Choi, Bu-Mahn Park, Jeonghwan Hwang, Miyoung Park

{"title":"Inhibitory Effect of a Novel Non-Steroidal AMPamide on Inflammation and Sebogenesis by Suppressing TLR4 and TLR6-Mediated Signaling Pathway.","authors":"Myo Hyeon Park, Yu Ra Jung, Eun Bi Choi, Bu-Mahn Park, Jeonghwan Hwang, Miyoung Park","doi":"10.4062/biomolther.2025.072","DOIUrl":"10.4062/biomolther.2025.072","url":null,"abstract":"Seborrheic dermatitis (SD) is a chronic inflammatory skin disorder that primarily affects areas with increased sebaceous gland activity, and is characterized by erythematous scaly lesions. Malassezia utilizes sebum lipids to produce free fatty acids that may disrupt the epidermal barrier and trigger inflammation in eczematous lesions. However, the pathogenesis and mechanisms underlying the exaggerated inflammatory response and sebogenesis regulation in SD remain unknown. Activation of pattern recognition receptors, including Toll-like receptors (TLRs), is crucial for initiating innate immunity. In the present study, we evaluated the efficacy of a novel antimicrobial cosmetic ingredient, AMPamide, and elucidated its molecular mechanisms underlying the suppression of inflammation and sebogenesis in SD. Specifically, we investigated the inhibitory effect of AMPamide on TLR activation and its impact on downstream signaling pathways in LPS-stimulated HaCaT cells. The effects of AMPamide on lipid production and the expression of related regulatory factors in IGF-1-stimulated SZ95 sebaceous gland cells were also examined. These analyses were performed using RT-qPCR, western blotting, immunofluorescence staining, and Nile Red staining. AMPamide exhibited anti-inflammatory and skin barrier-strengthening effects by inhibiting TLR4/6 expression and multiple signaling pathways. Additionally, AMPamide attenuated lipid overproduction and the expression of related regulatory factors in IGF-1-stimulated SZ95 sebaceous gland cells. Therefore, the observed effects of AMPamide on LPS-stimulated human keratinocytes were mediated via blockade of the TLR-MyD88-MAPK and NF-κB signaling pathway. These results revealed that AMPamide may be a potential therapeutic agent for SD that inhibits TLR4/6 activation.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"866-875"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788180","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

Arrestins as Possible Drug Targets. 逮捕是可能的毒品目标。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-06 DOI: 10.4062/biomolther.2025.079

Zeynep Nur Cinviz, Elisabetta Moroni, Ozge Sensoy, Giulia Morra, Vsevolod V Gurevich

引用次数: 0

Pathophysiological Insights and Clinical Management Strategies for Interstitial Lung Diseases. 间质性肺疾病的病理生理学见解和临床管理策略。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-14 DOI: 10.4062/biomolther.2025.003

Lin Tian, Yun Wang, Wenlong Qi, Bingsen Wang, Xudong Zhang, Mingxue Gong, Xiang Zhang, Tan Wang

{"title":"Pathophysiological Insights and Clinical Management Strategies for Interstitial Lung Diseases.","authors":"Lin Tian, Yun Wang, Wenlong Qi, Bingsen Wang, Xudong Zhang, Mingxue Gong, Xiang Zhang, Tan Wang","doi":"10.4062/biomolther.2025.003","DOIUrl":"10.4062/biomolther.2025.003","url":null,"abstract":"Interstitial lung disease (ILD) represents a heterogeneous group of diseases in which inflammation and/or fibrosis in the pulmonary interstitium results in an impaired gas exchange, difficulties in breathing, and reduced quality of daily life, and contributes to elevated global morbidity and mortality rates. ILD is an umbrella term, with idiopathic pulmonary fibrosis (IPF) being a prime focus because of its progressive and severe form. Out of 300 underlying etiologies, ILD is one of the major reasons for global morbidity and mortality. This review offers a comprehensive overview of six main categories of ILD covering autoimmune, idiopathic interstitial pneumonia, hypersensitivity pneumonitis, drug-induced, infection-related, and unclassified ILD that underscore the complexity of diagnosis and treatment challenges. This review also provides an evidence-based overview of recent advancements in the diagnosis and management of ILD, with precision pharmacotherapy, multidisciplinary care, and emerging therapeutic strategies. From clinical trial data, it also recommends the disease-specific use of pharmacological agents-such as pirfenidone and nintedanib for IPF, and mycophenolate mofetil for connective tissue disease-associated ILD. The manuscript also emphasizes the evolving role of non-pharmacological interventions, including the 6-minute walk test and pulmonary rehabilitation, in enhancing functional capacity and quality of life. To address the current global health concerns, topics of post-COVID-19 ILD and immune checkpoint inhibitor-associated lung disease are integrated. Additionally, future directions are explored, including the role of lung transplantation and novel antifibrotic therapies like anti-Transforming Growth Factor (TGF)-β antibody cocktails. Together, these insights aim to refine diagnostic precision, personalize treatment, and improve clinical outcomes across the heterogeneous ILD spectrum.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"785-803"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144844326","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