Korean Journal of Physiology & Pharmacology最新文献

{"title":"Agmatine decreases long-term potentiation <i>via</i> α2-adrenergic receptor and imidazoline type 1 receptor in the hippocampus.","authors":"Wonseok Chang, Jihua An, Sang Hyun Jang, Moonil Kim, Sun Seek Min","doi":"10.4196/kjpp.24.399","DOIUrl":"https://doi.org/10.4196/kjpp.24.399","url":null,"abstract":"<p><p>Agmatine, a decarboxylation product of L-arginine, has been proposed as a novel neurotransmitter/neuromodulator with diverse neuroprotective and antidepressant-like effects. Although its therapeutic potential has been explored, the precise mechanisms by which agmatine modulates synaptic transmission and plasticity in the hippocampus remain unclear. In this study, we investigated the effects of agmatine on the induction and maintenance of long-term potentiation (LTP) in the CA1 region of mouse hippocampal slices, its ability to counteract amyloid-β (Aβ1-42)-induced LTP impairment, and the receptor systems involved. Bath application of agmatine significantly suppressed the maintenance phase of LTP. Notably, agmatine reversed Aβ-induced deficits in LTP, suggesting a protective effect against synaptic dysfunction. Pharmacological experiments demonstrated that these effects were mediated <i>via</i> α2-adrenergic and imidazoline type I receptors. Paired-pulse facilitation and input-output analyses revealed that agmatine did not alter presynaptic release probability but selectively modulated postsynaptic transmission, particularly under AMPA receptor blockade, indicating a potential regulation of NMDA receptor-mediated signaling. Together, these findings suggest that agmatine modulates hippocampal synaptic plasticity through receptor-specific, postsynaptic mechanisms, and highlight its potential as a therapeutic agent against synaptic impairments in neurodegenerative diseases.</p>","PeriodicalId":54746,"journal":{"name":"Korean Journal of Physiology & Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144735523","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":"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":"https://doi.org/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":""},"PeriodicalIF":2.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tie2 activator 4E2 ameliorates diabetic nephropathy and synergizes with dapagliflozin in a mouse model.","authors":"Da Som Jeong, Soo Min Ko, Ji-Young Lee, Hyo-Jeong Han, Yerin Lee, Weon Sup Lee, Eun-Ah Lee, Woo-Chan Son, Jinho Shin","doi":"10.4196/kjpp.24.424","DOIUrl":"https://doi.org/10.4196/kjpp.24.424","url":null,"abstract":"<p><p>Diabetic nephropathy (DN), a primary cause of end-stage renal disease, stems from hyperglycemia-induced vascular dysfunction and aberrant angiogenesis. Sodium-glucose cotransporter 2 inhibitors, such as dapagliflozin, improve glycemic control and provide renal protection yet fall short of fully halting DN progression. This study explores 4E2, a Tie2 receptor activator that mimics angiopoietin-1 to stabilize the vascular endothelium, as a novel DN therapy-both independently and in combination with dapagliflozin. In a streptozotocin (STZ)-induced DN mouse model (DBA/2J strain), male mice were treated with weekly intravenous 4E2, daily oral dapagliflozin, or a combination of both for 4 weeks following STZ administration. Dapagliflozin primarily reduced fasting blood glucose with modest renoprotective effects, whereas 4E2 significantly lowered kidney weight, blood urea nitrogen, and urinary albumin while elevating serum albumin, indicating greater renal protection. Histological analysis showed that 4E2 more effectively attenuated glomerular hypertrophy and lesions compared to dapagliflozin. Immunohistochemistry revealed that 4E2 markedly increased VE-cadherin and CD31 expression while decreasing PDGFR-β, reflecting enhanced endothelial stability and reduced vascular remodeling through Tie2-mediated mechanisms. Combination therapy synergistically enhanced these outcomes, achieving superior reductions in glucose levels, glomerular damage, and vascular pathology compared to either treatment alone. In contrast to anti-VEGF therapies, which can worsen proteinuria, 4E2-mediated Tie2 activation normalizes vascular stability without disrupting physiological angiogenesis, providing a safer therapeutic option. These findings establish 4E2 as a promising treatment for DN, especially when combined with dapagliflozin, by leveraging Tie2-driven stabilization and synergistic benefits to meet this critical unmet need.</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":"144709957","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":"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":"https://doi.org/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":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","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":"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":"https://doi.org/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":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA circAtxn10 regulates skeletal muscle cell differentiation by targeting miR-143-3p and Chrna1.","authors":"Nakwon Choe, Anna Jeong, Hosouk Joung, Dongtak Jeong, Young-Kook Kim, Hyun Kook, Duk-Hwa Kwon","doi":"10.4196/kjpp.25.046","DOIUrl":"https://doi.org/10.4196/kjpp.25.046","url":null,"abstract":"<p><p>Skeletal muscle differentiation is a complex process regulated by a network of genes and transcription factors. Recent studies have revealed the roles of circular RNAs (circRNAs) and microRNAs (miRNAs) in modulating gene expression during myogenesis. In this study, we focused on the functional interplay between circAtxn10, miR-143-3p, and the nicotinic acetylcholine receptor subunit alpha 1 (Chrna1) in skeletal muscle differentiation. Our results demonstrate that circAtxn10 expression increases during myogenic differentiation and acts as a sponge for miR-143-3p through direct binding. We identified Chrna1 as a direct target of miR-143-3p through three binding sites in its 3'-UTR and showed that both miR-143-3p mimic and Chrna1 knockdown significantly impair myogenesis. Notably, Chrna1 overexpression dramatically enhanced myogenic marker expression and myotube formation. Our findings establish a regulatory axis involving circAtxn10, miR-143-3p, and Chrna1 that plays a critical role in modulating skeletal muscle differentiation, providing new insights into the complex molecular mechanisms regulating myogenesis.</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":"144700388","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":"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":"https://doi.org/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":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","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}