Clinical science最新文献

{"title":"Overexpression of TrpC5 promotes tumor metastasis via the HIF-1α/Twist signaling pathway in colon cancer.","authors":"","doi":"10.1042/CS20171069_RET","DOIUrl":"10.1042/CS20171069_RET","url":null,"abstract":"","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 11","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apolipoprotein-L1 G1 variant contributes to hydrocephalus but not to atherosclerosis in apolipoprotein-E knock-out mice.","authors":"Teruhiko Yoshida, Zhi-Hong Yang, Shinji Ashida, Zu Xi Yu, Shashi Shrivastav, Krishna Vamsi Rojulpote, Piroz Bahar, David Nguyen, Danielle A Springer, Jeeva Munasinghe, Matthew F Starost, Victoria J Hoffmann, Avi Z Rosenberg, Bibi Bielekova, Han Wen, Alan T Remaley, Jeffrey B Kopp","doi":"10.1042/CS20255324","DOIUrl":"10.1042/CS20255324","url":null,"abstract":"<p><p>In USA, six million individuals with Sub-Saharan ancestry carry two APOL1 high-risk variants, which increase the risk for kidney diseases. Whether APOL1 high-risk variants increase other diseases under dyslipidemia remains unclear and requires further investigation.We characterized a mouse model to investigate the role of APOL1 in dyslipidemia and cardiovascular diseases. Transgenic mice carrying APOL1 (G0 and G1 variants)on bacterial artificial chromosomes (BAC/APOL1 mice) were crossed with the ApoE knock-out (ApoE-KO) dyslipidemia and atherosclerosis mouse model. The compound transgenic mice were evaluated for the impact of APOL1 on systemic phenotypes. ApoE-KO mice carrying APOL1-G0 and APOL1-G1 did not show differences in the extent of atherosclerotic lesions or aortic calcification, as evaluated by Sudan IV staining and radiographic examination, respectively. However, ~20% of ApoE-KO; BAC/APOL1-G1 mice developed hydrocephalus and required euthanasia. The hydrocephalus was communicating and likely was due to excess cerebrospinal fluid produced by the choroid plexus, where epithelial cells expressed APOL1. Single-nuclear RNA-seq of choroid plexus identified solute transporter upregulation and mTORC2 pathway activation in APOL1-G1-expressing epithelial cells. Further, in the All of Us cohort, we found higher hydrocephalus prevalence among individuals with the APOL1-G1 variant in both recessive and dominant models, supporting the mouse findings. While APOL1-G1 expression in ApoE-KO mice did not worsen cardiovascular disease phenotypes, we uncovered hydrocephalus as a novel APOL1 risk allele-mediated phenotype. These findings extend the spectrum of APOL1-associated pathologies.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reductions in angiotensin II type 2 receptor-mediated vasodilation contribute to increased angiotensin II vasoconstrictor sensitivity in women with preeclampsia history.","authors":"Kelsey Schwartz, Nathan Campbell, Diana Jalal, Anna Stanhewicz","doi":"10.1042/CS20245238","DOIUrl":"10.1042/CS20245238","url":null,"abstract":"<p><p>Women with a history of preeclampsia (hxPE) have a ≥4-fold risk for developing cardiovascular disease (CVD) compared with women who had a healthy pregnancy (hxHC). HxPE have exaggerated vasoconstrictor sensitivity to angiotensin (ang) II after pregnancy, which likely contributes to CVD progression after preeclampsia. Ang II-mediated constriction via ang II type 1 receptors (AT1R) is countered by vasodilatory ang II type 2 receptors (AT2R); however, the extent that reductions in AT2R-mediated responses contribute to exaggerated ang II-mediated constriction after preeclampsia is unknown. We examined the balance of AT1R- and AT2R-mediated responses in hxPE and hxHC (n=12/group). We hypothesized that 1) attenuated AT2R-mediated dilation would be improved with AT1R inhibition in hxPE, and 2) AT2R inhibition would increase ang II-mediated constriction in hxHC but have no effect in hxPE. We measured cutaneous vascular conductance responses to compound 21 (AT2R agonist; 10-14-10-8mol/L) alone or with losartan (AT1R antagonist; 43µmol/L) to assess AT2R-mediated dilation, and ang II (10-20-10-4mol/L) alone or with PD-123319 (AT2R antagonist; 1µmol/L) to assess the role of AT2R in vasoconstrictor sensitivity to ang II. Reduced AT2R-mediated dilation in hxPE (P=0.002) was improved with AT1R inhibition (P<0.001). Vasoconstrictor sensitivity to ang II was greater in hxPE compared with hxHC (P<0.001). Circulating AT1R agonistic autoantibodies (AT1-AA) were elevated in hxPE (P=0.015). AT2R inhibition increased the vasoconstrictor response to ang II in hxHC (P<0.001) but had no effect in hxPE (P=0.19). These data suggest that hxPE have reduced AT2R-mediated dilation that contributes to increased ang II vasoconstrictor sensitivity after preeclampsia.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering complexity of GPCR signaling and modulation: implications and perspectives for drug discovery.","authors":"Claudio M Costa-Neto, Lucas T Parreiras-E-Silva","doi":"10.1042/CS20245182","DOIUrl":"10.1042/CS20245182","url":null,"abstract":"<p><p>G protein-coupled receptors (GPCRs) are central to pathophysiological processes and remain prominent targets in drug discovery. Recent advances in understanding GPCR signaling and modulation, such as biased agonism, dual agonism, and non-canonical G protein signaling, have expanded the therapeutic landscape of these receptors. These understandings have led (and are leading further) to innovative approaches that broaden GPCRs as therapeutic targets, going after better efficacy and minimizing adverse effects. However, tachyphylaxis, a rapid decrease in receptor responsiveness after repeated stimulation, presents a significant challenge in a chronic treatment context. Recent findings from our group revealed that tachyphylaxis in the angiotensin type 1 (AT1) receptor is primarily governed by the ligand's dissociation rate (koff), i.e. high residence time, rather than by β-arrestin-mediated desensitization, as could be expected. This suggests that internalized AT1 receptors remain active when bound to ligands with high residence time, favoring sustained signaling from endosomes. Importantly, the concept of high residence time sheds new light on intracellular signaling phenomena and underscores the therapeutic value of modulating intracellular receptor activity, including the development of novel cell-permeant antagonists. This review discusses critical pharmacological parameters for drug discovery focused on agonists, including (i) activation of preferential signaling pathways (biased agonism), (ii) internalization/recycling rates, (iii) tachyphylaxis/desensitization, (iv) allosteric modulators, and (v) intracellular receptor signaling and its blockade, emphasizing the need for strategies that extend beyond conventional GPCRs' functional assays. Additionally, this review highlights how advancements in high-resolution imaging, bioluminescence resonance energy transfer-based biosensors, and computational modeling are crucial for elucidating complex GPCRs' behaviors, particularly in understanding mechanisms like tachyphylaxis and its interplay with compartment-specific signaling. These approaches not only pave the way for therapies that strategically leverage or mitigate tachyphylaxis to sustain receptor responsiveness, but could enable the design of drugs targeting intracellular pathways as a strategy to enhance efficacy and minimize adverse effects. These insights underscore the importance of integrating diverse pharmacological strategies to refine GPCR-targeted therapies and address unmet medical needs, particularly in chronic conditions where sustained receptor activity is critical.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 10","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LONP1 facilitates pulmonary artery smooth muscle cell glycolytic reprogramming by degrading MPC1 in pulmonary hypertension.","authors":"Mingkang Li, Wenkang Zhang, Minhao Zhang, Linqing Li, Yuyu Yao, Yuhan Qin, Dong Wang, Gaoliang Yan, Yong Qiao, Chengchun Tang","doi":"10.1042/CS20255922","DOIUrl":"10.1042/CS20255922","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is a chronic and life-threatening disease characterized by pulmonary vascular remodeling (PVR), which involves the abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs). These cells exhibit metabolic characteristics akin to cancer cells, particularly in their shift toward glycolysis. The Lon protease 1 (LONP1) has been shown to promote glycolytic reprogramming of tumor cells, conferring a malignant proliferative phenotype. However, the precise role of LONP1 in PH remains unclear. In the present study, Su5416/hypoxia-induced and monocrotaline (MCT)-induced PH rodent models and platelet-derived growth factor BB (PDGF-BB)-induced PASMCs were used to investigate the role and mechanism of LONP1 in PH. The results revealed an up-regulation of LONP1 expression in lung tissues from two PH rodent models, as well as in PDGF-BB-induced PASMCs. In vivo knockdown of LONP1 significantly alleviated PASMC mitochondrial dysfunction, reduced glycolytic enzyme expression, and decreased lactate accumulation, thereby mitigating PVR. Additionally, in vitro experiments demonstrated that knockdown or inhibition of LONP1 attenuated glycolytic reprogramming, proliferation, and migration of PASMCs, whereas overexpression of LONP1 had converse effects. Mechanistic studies confirmed that mitochondrial pyruvate carrier 1 (MPC1) was a direct substrate for LONP1-mediated degradation. Functional experiments with MPC1 knockdown and overexpression further elucidated its role in the proliferation and migration of PASMCs. Rescue experiments indicated that MPC1 knockdown abrogated the suppressive effects of LONP1 knockdown on glycolytic reprogramming, proliferation, and migration in PASMCs. Therapeutically, knockdown or pharmacological inhibition of LONP1 significantly reversed MCT-induced PH in rats. Thus, targeting LONP1 may represent a promising therapeutic strategy for PH.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased absorptive transcytosis and tight junction weakness in heart failure are equally corrected by exercise training and losartan.","authors":"Hiviny de Ataides Raquel, Mariana Makuch-Martins, Sany M Perego, Gustavo S Masson, Leonardo Jensen, Lisete C Michelini","doi":"10.1042/CS20242965","DOIUrl":"10.1042/CS20242965","url":null,"abstract":"<p><p>Reduced ventricular function, renin-angiotensin system upregulation and sympathoexcitation are hallmarks of heart failure (HF). Recently we showed that blood-brain barrier (BBB) lesion within autonomic nuclei contributes to autonomic imbalance and that exercise training (T) normalizes BBB function and improves autonomic control. We sought now to identify the mechanism( involved in both HF-induced lesion and exercise-induced correction. Wistar rats submitted to coronary artery ligation were, after the development of HF, assigned to losartan (Los) or vehicle (Veh) treatments and simultaneously submitted to T or sedentary ( protocol. After hemodynamic/autonomic recordings and evaluation of BBB permeability, brains were harvested for ultrastructural analyses of the barrier (tight junctions (TJ) tightness and vesicles trafficking) within capillaries of the hypothalamic paraventricular nucleus. Local angiotensin II (Ang II) expression and activation of microglial cells (IBA-1 immunofluorescence) were also evaluated. High sympathetic activity and pressure variability, reduced parasympathetic control of the heart, elevated BBB permeability, high vesicular trafficking and TJ weakness exhibited by Veh-rats were equally corrected in Veh-T, Los-and Los-T groups. The increased PVN Ang II expression and IBA-1 density in Veh-group were similarly reduced by T, Los and combination of both. Ang II, colocalized with microglia AT1 receptors, induced their remodeling from disease-associated phenotype in Veh-S rats to homeostatic-surveilling conditions in the other groups. All measured parameters exhibited strong correlations with Ang II availability. Data indicated that changes in PVN Ang II availability induced by HF, exercise and losartan is the key regulator of transcellular and paracellular transport across the BBB.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Physiological response to fetal intravenous lipid emulsion.","authors":"","doi":"10.1042/CS20231419_COR","DOIUrl":"10.1042/CS20231419_COR","url":null,"abstract":"","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 10","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12224897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum proteomics links the cardiorespiratory biomarkers CTRC, OSM, and MMP-10 to exacerbation severity and number in patients with COPD.","authors":"Eduardo I Cardenas, Kristina Andelid, Nikolaos Pournaras, Ann Ekberg- Jansson, Nicola Orsini, Georgios Stratelis, Tomas Jernberg, Anders Lindén","doi":"10.1042/CS20255852","DOIUrl":"10.1042/CS20255852","url":null,"abstract":"<p><p>During exacerbations, patients with chronic obstructive pulmonary disease (COPD) are at risk for severe cardiovascular disease (CVD). Despite this, the available literature on systemic biomarkers of CVD during exacerbations is limited. In the present study, a proteomic approach was used to assess alterations in the concentrations of 177 biomarkers of CVD and inflammation in serum samples from 26 long-term smokers (LTS) with mild-to-severe COPD (GOLD stage 1-3) and chronic bronchitis (COPD-CB) but no allergy. These patients were followed for 60 weeks, and they all provided paired samples during stable disease and exacerbations. Serum samples from ten healthy non-smokers (HNS) and ten LTS without COPD or CB constituted controls. Of all the proteins analyzed, only chymotrypsin C (CTRC), oncostatin M (OSM), and matrix metalloproteinase 10 (MMP-10) displayed significantly altered concentrations during exacerbations in the COPD-CB group. Here, the concentrations of CTRC and OSM correlated with exacerbation severity, CRP, blood leukocytes, and other cardiovascular biomarkers. In contrast, the concentration of MMP-10 during stable disease correlated with blood eosinophil counts and exacerbation numbers. Finally, the concentrations of OSM and MMP-10 during stable disease correlated with blood leukocytes and tobacco load, respectively. Our study suggests that CTRC, OSM, and MMP-10 bear potential as cardiorespiratory biomarkers in patients with COPD and CB. Collectively, these biomarkers display substantial alterations during exacerbations and correlate with the severity and number of exacerbations. These results motivate prospective studies to determine the clinical utility of CTRC, OSM, and MMP-10 in assessing cardiorespiratory risk in patients with COPD.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 9","pages":"449-462"},"PeriodicalIF":6.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-talk between microbiota-gut-brain axis and blood pressure regulation.","authors":"Malindi Welathanthree, Damien J Keating, Vaughan G Macefield, Daniela Carnevale, Francine Z Marques, Rikeish R Muralitharan","doi":"10.1042/CS20240787","DOIUrl":"10.1042/CS20240787","url":null,"abstract":"<p><p>Hypertension, or high blood pressure (BP), is a widespread condition affecting one in three adults globally. Despite the availability of treatment options, 50% of hypertensive patients in countries such as Australia fail to achieve adequate BP control, often due to a lack of response to current therapies. Diet plays a crucial role in BP regulation. A high-fibre diet reduces BP through the gut microbiome and the production of microbial metabolites known as short-chain fatty acids (SCFAs). However, the mechanisms of BP regulation by SCFAs remained still unclear. A novel hypothesis we explore in this review is that these microbial metabolites may regulate BP via the activation of central mechanisms, a phenomenon called the gut-brain axis. While substantial evidence in animal models and humans supports the protective role of SCFAs in hypertension, the precise mechanisms remain unclear. SCFA stimulates the release of neurotransmitters and hormones such as serotonin, cholecystokinin, glucagon-like peptide 1 and peptide YY by enteroendocrine cells, a rare population of cells lining the gastrointestinal tract. These hormones bind to their receptors on the peripheral nervous system nerves, such as the vagus and spinal nerves, conveying information to the brain. The mechanisms by which information is relayed from the gut microbiome to the brain likely involve the immune system and gut-derived neurotransmitters and hormones. A deeper understanding of these pathways and mechanisms will facilitate the development of novel therapeutics for hypertension and other cardiovascular diseases.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 9","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin II-induced cardiac fibrosis and dysfunction are exacerbated by deletion of cGKI in periostin+ myofibroblasts.","authors":"Melanie Cruz Santos, Lena Birkenfeld, Thomas Pham, Selina Maier, Katharina Paulus, Lena Ullemeyer, Amelie Knauer, Clement Kabagema-Bilan, Natalie Längst, Anna Roslan, Nina Wettschureck, Meinrad Gawaz, Fumito Ichinose, Robert Lukowski","doi":"10.1042/CS20241204","DOIUrl":"10.1042/CS20241204","url":null,"abstract":"<p><p>Differentiation of cardiac fibroblasts (CF) into myofibroblasts (CMFs) is considered a critical event in response to the maladaptive cardiac remodeling triggered by angiotensin II (Ang II). Active CMFs are proliferative and contribute to the production of extracellular matrix and matricellular proteins such as periostin, to myocardial fibrosis and thus muscle stiffness. Although previous studies provided substantial evidence for the antifibrotic signaling elicited by NO/NP-cGMP-cGKI, the role of this axis in modulating CMF function(s) in vivo remains unclear.To address this, Ang II was delivered through osmotic minipumps into tamoxifen-induced CMF-specific cGKI knockout (cmfKO) and littermate control (CTR) male mice. CMF-restricted Cre activity in periostin+ cells resulted in an effective depletion of the cGKI protein observed in myocardial sections and in primary CF/CMF protein lysates obtained from Ang II-and tamoxifen-treated cmfKO. Although both genotypes responded identically to Ang II in terms of blood pressure and cardiac enlargement, cmfKO hearts showed significantly increased cardiomyocyte cross-sectional areas and developed a marked increase in myocardial fibrosis. Moreover, non-invasive echocardiography revealed a structure-related distortion of global systolic function and longitudinal deformation capacity in cmfKO versus CTR. Consistent with the results obtained in vivo, we observed a higher proliferation rate of CF/CMF derived from Ang II-treated cmfKO hearts compared to respective CTR cells as well as an increase in cardiomyocyte apoptosis in the absence of cGKI in periostin+ CMF. Our data confirm that endogenous cGKI function in periostin+ CMFs counteracts the Ang II-induced morphologic and structural changes that impair cardiomyocyte survival ultimately causing loss of heart function in male mice.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":6.7,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}