Korean Journal of Physiology & Pharmacology最新文献

{"title":"Procyanidin B2-induced LKB1-AMPK activation mitigates vascular smooth muscle cell proliferation through inhibition of mTOR signaling.","authors":"Hee Young Park, Seul Gi Kim, Gyeong Ju Bae, Jin Young Sung, Hyoung Chul Choi","doi":"10.4196/kjpp.25.108","DOIUrl":"10.4196/kjpp.25.108","url":null,"abstract":"<p><p>Vascular smooth muscle cell (VSMC) proliferation contributes to intimal thickening in atherosclerosis and restenosis diseases. As a proanthocyanidin type B, procyanidin B2 (PB2) is abundantly found in cocoa, apples, and grapes and is reported to have vascular protective effects. However, the mechanisms by which PB2 inhibits proliferation of VSMCs are not clearly understood. Therefore, the purpose of this study was to investigate the underlying mechanism of PB2-induced inhibition of cell proliferation in VSMCs. We found that PB2 dose- and time-dependently increased phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK) in VSMCs. AMPK is a serine-threonine kinase and serves as a key sensor of cellular energy. PB2 induced LKB1 translocation from nucleus to cytosol which led to AMPK activation. In addition, PB2-induced AMPK activation decreased cell proliferation and cell cycle progression by inhibiting mammalian target of rapamycin signaling pathway. Transfection with LKB1 or AMPK siRNA and transduction of dominant-negative isoforms of the α1 and α2 subunits of AMPK eliminated anti-proliferative effects of PB2. These results demonstrate that PB2 might be a preventive agent for cardiovascular disorders such as atherosclerosis and hypertension.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"659-667"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amorfrutin A ameliorates cerebral ischemia/reperfsion injury <i>in vivo</i> and <i>in vitro via</i> modulating Nrf2/HO-1 signaling pathway.","authors":"Youxi Yang, Liying Shi, Xiaoting Xu, Bilan Luo, Xing Cui, Lei Tang, Jianta Wang","doi":"10.4196/kjpp.24.304","DOIUrl":"10.4196/kjpp.24.304","url":null,"abstract":"<p><p>Ischemic stroke is a leading cause of death and disability worldwide. Amorfrutin A (AA), a small molecule compound found in <i>Amorpha fruticosa</i> L. (bastard indigo), possesses various activities, including blood glucose regulation, antiinflammatory, analgesic, and tumor suppression. In this study, we used the middle cerebral artery occlusion/reperfusion (MCAO/R) model and the oxygen glucose deprivation/ reoxygenation (OGD/R) model to mimic the ischemia/reperfusion process <i>in vivo</i> and <i>in vitro</i>, respectively. The role of AA in ischemic stroke was evaluated by CCK-8 assay, ELISA, TTC staining, hematoxylin-eosin staining and Western blot assay. AA increased the survival of BV2 or PC12 cells following OGD/R injury. Meanwhile, AA effectively suppressed the release of reactive oxygen species, nitric oxide, and tumor necrosis factor-α (TNF-α) in BV2 or PC12 cells subjected to OGD/R. After 24 h of MCAO/R surgery, AA significantly reduced the neurological deficit score, diminished the cerebral infarct volume, and attenuated brain pathological injury in rats. AA administration significantly increased superoxide dismutase and glutathione peroxidase levels, reduced malondialdehyde production, and inhibited the release of inflammatory cytokines interleukin-1β and TNF-α in the ischemic brain tissue of MCAO/R rats. In addition, AA suppressed Kelch-like ECH-associated protein 1 expression and promoted nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H quinone oxidoreductase 1, and heme oxygenase 1 (HO-1) expression in rat ischemic brain. AA may be a potential drug for the treatment of ischemic stroke. Its antioxidant and anti-inflammatory effects in cerebral ischemia-reperfusion injury may be related to Nrf2/HO-1 signaling pathway.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"547-557"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-related changes in diurnal expression of inflammatory mediators in the brain and peripheral blood of male and female mice.","authors":"Eun-Mi Lee, Hyun-Jung Kim, Yelin Park, Jihee Lee Kang, Eun-Mi Park","doi":"10.4196/kjpp.24.372","DOIUrl":"10.4196/kjpp.24.372","url":null,"abstract":"<p><p>Several molecules in human body exhibit light-dependent diurnal expression rhythms, and their disruption impairs physiological functions and health. Normal aging alters these rhythms, contributing to aging processes and age-related brain disorders. Chronic low-grade inflammation is a hallmark of aging (inflammaging), and age-related changes in the diurnal expression of proinflammatory cytokines have been reported in the suprachiasmatic nucleus (SCN) and peripheral blood. However, it remains unclear which genes show diurnal expression changes in brain with the SCN regions removed (extra-SCN) and whether these changes are reflected in peripheral blood. To address this, we analyzed the diurnal expression of genes in extra-SCN brain regions and cytokines in the peripheral blood of young and aged male and female mice. Samples were collected during the light (10 AM) and the dark (10 PM) phases and analyzed using RNA sequencing and cytokine array analysis. In the aged brain, the number of genes displaying diurnal variation in expression was reduced, whereas genes related to inflammation and immune responses, especially <i>Ccl21</i>, were upregulated regardless of phase, suggesting age-associated immune dysregulation. However, peripheral blood levels of CCL21 protein did not differ between age groups. Instead, CXCL13 and IGFBP1 showed age-related diurnal alterations in the blood, but their expression patterns in the aged brain differed from those in the blood. These findings indicate that diurnal expression of inflammation-related molecules is altered with aging in both the brain and blood, with differences observed. These diurnal changes may contribute to the underlying mechanism of inflammaging and age-related diseases.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"559-570"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144709955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of Xuefu Zhuyu decoction in treating diabetic kidney disease-induced renal fibrosis: UPLC-Q/TOF-MS, network pharmacology, and experimental validation.","authors":"Yifei Zhang, Shuaixing Zhang, Zeyu Zhang, Zijing Cao, Xuehui Bai, Shujiao Zhang, Mengqi Zhou, Jingyi Tang, Yiran Xie, Zhongjie Liu, Weijing Liu, Yuning Liu","doi":"10.4196/kjpp.24.330","DOIUrl":"10.4196/kjpp.24.330","url":null,"abstract":"<p><p>Xuefu Zhuyu decoction (XFZY) has therapeutic effects on diabetic kidney disease (DKD)-induced renal interstitial fibrosis (RIF), but the mechanisms are unclear. This study investigates XFZY's molecular mechanisms through network pharmacology and experimental validation. Ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) and database screening was used to identify XFZY bioactive compounds. Common targets between these compounds and DKD-induced RIF were analyzed. A protein-protein interaction network was constructed, followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. Molecular docking validated interactions between XFZY compounds and targets. <i>In vivo</i>, a mouse model of DKD-induced RIF was established using streptozotocin and a high-fat diet. <i>In vitro</i>, human kidney-2 cells were treated with advanced glycation end products. Renal function and pathology were assessed, along with key protein expression levels. Using UPLC-Q-TOF-MS technology and database screening, seven bioactive components of XFZY were identified. Network pharmacology identified 61 common targets, including core targets like AKT1, MTOR, ULK1, and MMP9. Enrichment analysis indicated the AMPK signaling pathway is closely related to XFZY's therapeutic effects on DKD-induced RIF. Molecular docking demonstrated the seven bioactive components exhibited high binding affinities with key targets in the AMPK pathway (AMPK, mTOR, ULK1). <i>In vivo</i>, XFZY improved renal function, ameliorated renal pathology, reduced tubular injury, and alleviated RIF. Both <i>in vivo</i> and <i>in vitro</i>, XFZY increased phosphorylated AMPK and phosphorylated ULK1 expression, decreased phosphorylated MTOR, and reduced LC3 and p62 expression in the autophagy pathway. XFZY may alleviate DKD-induced RIF by modulating autophagy via the AMPK/MTOR/ULK1 pathway.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"571-597"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144735524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Organoid-based modeling and regenerative strategies for salivary gland dysfunction.","authors":"Hee-Jeong Park, Jaejin Cho, Su-Jeong Oh, Hyung-Sik Kim","doi":"10.4196/kjpp.25.149","DOIUrl":"https://doi.org/10.4196/kjpp.25.149","url":null,"abstract":"<p><p>Xerostomia, a pathological condition resulting from hyposalivation due to salivary gland (SG) dysfunction, severely affects a patient's health, quality of life, and healthcare costs. Despite its high prevalence, long-term curative treatments remain unavailable, leaving patients with lifelong symptom management. Permanent SG damage caused by disease or injury exacerbates this condition, highlighting the urgent need for regenerative solutions. Salivary gland organoids (SGOs) have emerged as promising <i>in vitro</i> models for studying SG homeostasis and pathology. SGOs serve as physiologically relevant three-dimensional models, enabling the study of tissue renewal, stem cell-niche interactions, and responses to genetic mutations, drugs, or injury. Additionally, advances in regenerative medicine, including stem cell-or organoid-based therapies integrated with bioengineering approaches, have the potential to develop future treatments. In this review, we summarize the latest progress in SGO development, explore its potential for modeling diseases and injuries, and discuss emerging regenerative strategies for restoring SG function. By deepening our understanding of SG physiology and diseases, these studies pave the way for therapeutic or regenerative approaches that have the potential to provide lasting relief for patients with xerostomia.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rewiring the scar: translational advances in cardiac fibrosis.","authors":"Tu Nguyen Tran, Phuoc Hoang Le, Seonbu Yang, Trang Luong, Jaetaek Kim","doi":"10.4196/kjpp.25.160","DOIUrl":"https://doi.org/10.4196/kjpp.25.160","url":null,"abstract":"<p><p>Cardiac fibrosis, characterized by excessive extracellular matrix accumulation and perpetual fibroblast activation, represents a common pathological endpoint across diverse cardiovascular diseases. Despite its central role in adverse cardiac remodeling and heart failure progression, targeted antifibrotic therapies remain largely elusive. This review synthesizes recent breakthroughs in understanding the molecular and cellular drivers of cardiac fibrosis, highlighting the complex interplay between fibrogenic signaling pathways, immune mechanisms, and extracellular matrix dynamics. We critically evaluate emerging diagnostic modalities from advanced imaging techniques to novel biomarker panels, emphasizing their translational potential and limitations. Current pharmacological approaches achieve only modest antifibrotic effects, whereas emerging targeted therapies such as small-molecule drugs, immunomodulatory agents, and cell-based strategies have shown promising results in preclinical models. The integration of precision medicine approaches with bioengineered platforms represents a paradigm shift in developing personalized antifibrotic interventions. This review provides a comprehensive framework for understanding the translational landscape of cardiac fibrosis and identifies critical gaps that must be addressed to advance effective therapies from bench to bedside.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OAC1 improves mitofusin 2 expression to alleviate neuronal injury following experimental ischemic stroke.","authors":"Yuanyuan Wang, Kechun Chen, Bingtian Xu, Haitao Wang, Honghao Wang, Tianming Lü","doi":"10.4196/kjpp.24.428","DOIUrl":"https://doi.org/10.4196/kjpp.24.428","url":null,"abstract":"<p><p>Recent research indicates that mitofusin 2 (MFN2) plays a pivotal role in the neuroprotective effects achieved by silencing nuclear receptor subfamily 6 group A member 1 (NR6A1) during cerebral ischemia. While NR6A1 is known to inhibit octamer-binding transcription factor 4 (OCT4), the regulatory relationship between OCT4 and MFN2 remains unknown. This study explores the neuroprotective effects of OCT4-activating compound 1 (OAC1), an OCT4 activator, against cerebral ischemia/reperfusion injuries and its underlying mechanism. In a murine stroke model, administration of OAC1 (3 mg/kg) significantly reduced brain infarction of mice and loss of MFN2. Notably, OAC1 treatment mitigated neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) in a dose-dependent manner. Additionally, OAC1 treatment also alleviated dysfunction of mitochondria and endoplasmic reticulum stress. Moreover, OAC1 application preserved both OCT4 and MFN2 expression following OGD/R, and MFN2 facilitate protective function of OAC1 against neuronal damage induced by OGD/R. Our results demonstrate that OAC1 can alleviate neuronal damage in cerebral ischemia by activating the OCT4/MFN2. These findings offer novel insights into MFN2 regulation and highlight OCT4's potential as a therapeutic target for cerebral ischemia.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144709956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fimepinostat is a dual inhibitor of tumor and angiogenesis in glioblastoma and synergizes with temozolomide through suppressing MYC.","authors":"Weifeng Wan, Xin Zhang, Hongcai Du, Changren Huang, Ligang Chen, Xiaobo Yang, Kunyang Bao","doi":"10.4196/kjpp.25.056","DOIUrl":"https://doi.org/10.4196/kjpp.25.056","url":null,"abstract":"<p><p>Glioblastoma, an aggressive brain tumor that largely depends on angiogenesis, has limited treatment options and poor prognosis. This study explores the therapeutic potential of fimepinostat, a dual HDAC/PI3K inhibitor, as a single agent alone and in combination of temozolomide in glioblastoma using preclinical tumor and angiogenesis models. We show that fimepinostat at nanomolar concentrations inhibited proliferation and induced apoptosis in a panel of glioblastoma cell lines. In addition, fimepinostat inhibited capillary network formation of microvascular endothelial cells derived from patients, indicating that fimepinostat inhibits glioblastoma angiogenesis. Combination index analysis indicates that fimepinostat and temozolomide is synergistic in inhibiting glioblastoma. Consistent with the <i>in vitro</i> findings, fimepinostat significantly inhibited glioblastoma growth in mice without causing any toxicity. The combination of fimepinostat and temozolomide significantly inhibited tumor growth and prolonged survival compared to monotherapy or control. Mechanism studies confirmed that fimepinostat acts on glioblastoma cells through suppressing Akt/MYC. Our findings suggest that dual targeting of tumor and angiogenesis by fimepinostat may provide an alternative approach for anti-glioblastoma therapy.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vericiguat reduces pyroptosis in rats with coronary microembolization by inhibiting the AMPK/Nrf2/NLRP3 signaling pathway.","authors":"Eksavang Khounphinith, You Zhou, Zeqiang Yi, Tao Li, Lang Li","doi":"10.4196/kjpp.25.008","DOIUrl":"https://doi.org/10.4196/kjpp.25.008","url":null,"abstract":"<p><p>Coronary microembolization (CME) is a prevalent and refractory complication of coronary revascularization, resulting in perioperative myocardial injury, cardiac dysfunction, and unfavorable prognosis. Vericiguat represents a novel therapeutic agent for chronic heart failure; however, further investigation is warranted to explore its potential cardioprotective effects beyond improving cardiac function in CME-induced myocardial injury. Therefore, the objective of this study is to evaluate the impact of vericiguat on pyroptosis in cardiomyocytes induced by CME and elucidate the underlying mechanism. The CME model was created in 40 Sprague-Dawley rats by injecting microspheres into the left ventricle, with the exception of the sham group. Vericiguat or CC (AMPK inhibitor), was given before creating CME models. Four groups were created for the rats: sham, CME, CME+VER, and CME+VER+CC, with random assignment. The CME+VER and CME+VER+CC groups received oral administration of vericiguat for a duration of two weeks before undergoing CME modeling. Echocardiography, myocardial histopathology, and serum markers of myocardial injury were assessed following induction of CME. Pyroptosis-related molecules and the adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor erythroid 2-like (Nrf2)/NOD-like receptor pyrin containing 3 (NLRP3) pathway were evaluated using qRT-PCR, Western blotting, ELISA, and immunofluorescence. Vericiguat pretreatment attenuated cardiac dysfunction and myocardial injury following CME. Furthermore, vericiguat ameliorates mitochondrial damage, facilitated AMPK activation, upregulated the expression of Nrf2, suppressed the initiation of the NLRP3 inflammasome and alleviated cardiomyocyte pyroptosis levels. However, the cardioprotective effects of vericiguat were reversed when co-treatment with CC. Vericiguat pretreatment reduces cardiomyocyte pyroptosis and myocardial injury after CME by activating the AMPK/Nrf2/NLRP3 pathway.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current view on the etiopathogenesis of aplastic anemia.","authors":"Mehmet Ali Ucar, Meryem Sener, Recep Dokuyucu","doi":"10.4196/kjpp.24.214","DOIUrl":"10.4196/kjpp.24.214","url":null,"abstract":"<p><p>Aplastic anemia (AA) is a rare bone marrow failure syndrome marked by hypocellular bone marrow and pancytopenia, typically without abnormal infiltration or reticulin fiber increase. It often presents as acute, severe cytopenia in young adults and can have high mortality if untreated. Recent advancements, including immunosuppressive therapy (IST) combined with eltrombopag and hematopoietic stem cell transplantation (HSCT), have improved patient outcomes. This review discusses current etiopathogenesis involving immune dysregulation, genetic mutations, and environmental triggers. Accurate differential diagnosis, distinguishing AA from myelodysplastic syndromes and paroxysmal nocturnal hemoglobinuria, is essential for effective treatment. We also highlight emerging therapies, such as mismatched unrelated donor (MMUD) transplantation and precision medicine targeting genetic abnormalities. AA, with an incidence of 2-4 per million annually, peaks at ages 15-25 and over 60. These insights continue to reshape AA prognosis and management. This disease typically manifests as acute, severe cytopenia, particularly in young adults, and has a high mortality rate if untreated. Advances in treatment, including IST combined with eltrombopag and HSCT, have significantly improved outcomes. In this review, we explore the current etiopathogenesis, including immune dysregulation, genetic mutations, and environmental factors. The differential diagnosis of AA, distinguishing it from conditions such as myelodysplastic syndromes and paroxysmal nocturnal hemoglobinuria, is critical for tailored treatment. AA remains a rare disease, with an annual incidence of 2-4 per million, and peaks in occurrence during the ages of 15-25 and over 60. These advancements in understanding and managing AA continue to transform its prognosis and patient care.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"399-408"},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}