Korean Journal of Physiology & Pharmacology最新文献

{"title":"Retraction to: Rehmannioside D mitigates disease progression in rats with experimental-induced diminished ovarian reserve <i>via</i> Forkhead Box O1/KLOTHO axis.","authors":"Yan Liang, Huimin Wang, Jin Chen, Lingyan Chen, Xiaoyong Chen","doi":"10.4196/kjpp.22.196rt","DOIUrl":"10.4196/kjpp.22.196rt","url":null,"abstract":"","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 6","pages":"781"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145373340","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":"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":"683-698"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576417/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.","authors":"Giang-Huong Vu, Byeong Hwa Jeon, Cuk-Seong Kim","doi":"10.4196/kjpp.25.236","DOIUrl":"10.4196/kjpp.25.236","url":null,"abstract":"<p><p>Diabetes mellitus is a major global health concern associated with micro-and macrovascular complications. Among the diverse mechanisms that contribute to vascular dysfunction in diabetes, endothelial to mesenchymal transition (EndMT) has emerged as a key pathological process. EndMT involves the loss of endothelial cell characteristics and the acquisition of mesenchymal features, resulting in impaired endothelial function, increased fibrosis, and inflammation. In addition to findings from preclinical models, recent human studies support the clinical relevance of End-MT. This review summarizes the molecular mechanisms governing EndMT, including key signaling pathways such as TGF-β, Notch, and Wnt, and examines how environmental, metabolic, and inflammatory cues influence this process. Furthermore, we discuss the maladaptive role of EndMT in diabetic complications, including nephropathy, retinopathy, atherosclerosis, and impaired wound healing, highlighting recent advances in anti-EndMT therapies and the clinical implications. Understanding the mechanisms of EndMT in the diabetic milieu may reveal novel therapeutic targets for preventing or reversing diabetic vascular diseases.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"699-711"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014423","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":"Poricoic Acid A attenuated TGF-β1-induced epithelial-mesenchymal transition in renal tubular epithelial cells through SPRY2/ERK signaling pathway.","authors":"Ming Xiang, Haiying Chen, Xiangdong Lin","doi":"10.4196/kjpp.24.384","DOIUrl":"10.4196/kjpp.24.384","url":null,"abstract":"<p><p>The progression of renal fibrosis is difficult to reverse, and Poria cocos, one of the main components of Wenyang Zhenshuai Granules, has been shown to be crucial to the development of the epithelial-mesenchymal transition (EMT). This study aimed to examine the molecular mechanism by which Poricoic Acid A (PAA) inhibited the advancement of EMT in renal tubular epithelial (RTE) cells. The protein levels of sprouty RTK signaling antagonist 2 (SPRY2) extracellular regulated protein kinases (ERK), and p-ERK were measured. The EMT progression of RTE cells was evaluated by a series of experiments. The regulatory relationship of PAA to SPRY2 was determined by cycloheximide, molecular docking and drug affinity target stability and immunoprecipitation. The overexpression of SPRY2 or PAA intervention suppressed the HK-2 and NRK-52E cell's viability, proliferation and migration ability of TGF-β1-induced while raising the levels of E-cadherin and decreasing those of collagen I, collagen III, Fibronectin1, α-SMA, Vimentin, ZEB1, Twist, Snail and Slug. PAA was able to be combined with SPRY2 protein. Besides, we found that PAA intervention increased the stability of SPRY2 through the ubiquitin-proteasome pathway, did not affect ERK levels, and reduced the levels of p-ERK. Finally, we found that inhibiting SPRY2 negated the beneficial effect of PAA on TGF-β1-stimulated RTE cells. PAA alleviated the EMT of RTE cells by modulating the SPRY2/ERK pathway.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"727-739"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014441","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":"Chick early amniotic fluid attenuates lipopolysaccharide-induced acute lung injury.","authors":"Chengxin Yin, Shan Lin, Jianzhou Li, Xiejiu Chen, Borui Li, Hui Yang, Baiping Cui","doi":"10.4196/kjpp.24.379","DOIUrl":"10.4196/kjpp.24.379","url":null,"abstract":"<p><p>Acute lung injury (ALI) and acute respiratory distress syndrome are major causes of acute respiratory failure and even death. Acute pneumonia can be accompanied by damage to the alveolar epithelium. <i>In vitro</i> functional experiments were performed by constructing inflammatory models in human alveolar epithelial cells. It was found that the chick early amniotic fluid (ceAF) extracted from SPF-grade early chicken embryos could significantly reduce the inflammation of human lung epithelial cells (Calu-3) induced by lipopolysaccharide (LPS) and COVID-19 protein pseudovirus, and reduce the gene expression of inflammatory factors. Pneumonia is one of the most common risk factors for causing ALI. An acute pneumonia model was constructed by LPS inhalation. Tail vein injection of ceAF significantly improved inspiratory and expiratory resistance, enhanced lung compliance, and reduced death rate due to acute pneumonia in mice. Neutrophil recruitment is an important feature of both acute inflammation and ALI. HE staining and immunohistochemical staining showed that ceAF treatment significantly reduced lung inflammatory edema and neutrophil cell aggregation, and promoted the resolution of inflammation in ALI, while reducing the inflammatory response in the blood. Further mass spectrometry experiments revealed that nicotinamide adenine dinucleotide (NAD⁺), guanosine and deoxyinosine were the primary components of ceAF. While each compound partially alleviated LPS-induced acute pneumonia, their effects were slightly weaker than those of ceAF, suggesting that ceAF's anti-inflammatory properties may arise from the synergistic action of these molecules.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 6","pages":"713-725"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145373299","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":"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":"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":"669-682"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576415/pdf/","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":"OA","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":"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":"755-767"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576420/pdf/","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":"OA","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":"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":"741-753"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576418/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction to: Edaravone alleviates lung damage in mice with hypoxic pulmonary hypertension by increasing nitric oxide synthase 3 expression.","authors":"Wan Zheng, Tianfa Li, Junping Wei, Yani Yan, Shanshan Yang","doi":"10.4196/kjpp.22.161rt","DOIUrl":"10.4196/kjpp.22.161rt","url":null,"abstract":"","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":"29 6","pages":"779"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12576419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145373297","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":"Hemistepsin A induces apoptosis by modulating the reactive oxygen species-dependent PI3K/Akt signaling pathway in human lung carcinoma A549 cells.","authors":"So Young Kim, Gi-Young Kim, Yung Hyun Choi","doi":"10.4196/kjpp.25.044","DOIUrl":"10.4196/kjpp.25.044","url":null,"abstract":"<p><p>Hemistepsin A is a sesquiterpene lactone isolated from plants of the family. Recently, this compound was reported to be a bioactive compound that is beneficial for numerous health problems without side effects; however, its effect on lung cancer cells has not yet been studied. Therefore, in this study, we investigated the anticancer activity of hemistepsin A in human lung carcinoma A549 cells. This study showed that treatment with hemistepsin A induces apoptosis by activating caspase cascade and reducing the expression of inhibitors of apoptotic protein family members. Additionally, hemistepsin A disrupted mitochondrial integration by altering the levels of Bcl-2 family proteins to increase the cytoplasmic release of cytochrome c. Moreover, hemistepsin A reduced the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, and pretreatment with a PI3K inhibitor markedly augmented the cytotoxic effect of hemistepsin A on A549 cells. Furthermore, hemistepsin A significantly enhanced the production of intracellular and mitochondrial reactive oxygen species (ROS), whereas ROS scavengers restored the reduced viability by attenuating DNA damage and apoptosis by blocking the hemistepsin A-mediated inactivation of the PI3K/Akt pathway. Our findings demonstrate that hemistepsin A induces apoptosis in A549 cells by generating ROS, which subsequently inhibits the PI3K/Akt pathway, suggesting that ROS generation is involved as an early inducer of hemistepsin A-mediated anticancer activity.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":"625-636"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700390","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}