Circulation research最新文献

{"title":"Micro(nano)plastics in the Development of Myocardial Fibrosis: From Clinical Detection to Molecular Mechanism.","authors":"Yilin Pan,Linqi Liu,Jiyuan Luo,Xiaozheng Zhou,Yu Wang,Lin Zheng,Yunxiao Yang,Zhan Peng,Jiawei Li,Guanming Su,Mianqi Xue,Kun Hua,Hanqing Chen,Xiubin Yang","doi":"10.1161/circresaha.125.327073","DOIUrl":"https://doi.org/10.1161/circresaha.125.327073","url":null,"abstract":"BACKGROUNDMicro(nano)plastics (MNPs) are pervasive environmental contaminants, yet their presence in human cardiac tissue and their potential contribution to myocardial fibrosis remain unclear. We investigated whether myocardial MNP burden is associated with fibrosis severity in patients and evaluated mechanistic plausibility in mice.METHODSLeft atrial appendage tissues were collected from patients undergoing cardiac surgery (n=33). MNP burden and polymer composition were quantified by pyrolysis-gas chromatography/mass spectrometry, and fibrosis was quantified histologically. In mice, 100-nm or 1-µm polystyrene nanoplastics were administered by oral gavage in coexposure and sequential exposure protocols with isoprenaline. Cardiac function was assessed by echocardiography, and fibrosis was evaluated by histology and immunohistochemistry. Transcriptomics, metabolomics, and 16S ribosomal RNA sequencing were performed to identify pathways linked to MNP exposure.RESULTSMNPs were detected in all human cardiac samples. Patients with high fibrosis exhibited higher total MNP levels than those with low fibrosis (171.74 [95% CI, 158.18-202.39] versus 119.33 [95% CI, 102.75-148.44] µg/g tissue; P=2.5×10-4), driven predominantly by elevated nanoplastics (122.83 [95% CI, 100.10-149.06] versus 86.39 [95% CI, 36.85-103.74] µg/g; P=0.010). Polystyrene and polyvinyl chloride were enriched in high-fibrosis tissues (polystyrene: P=3.3×10-4; polyvinyl chloride: P=0.002). Transcriptomics indicated activation of inflammatory and profibrotic pathways (TNF/NF-κB [nuclear factor-κB], TGF-β [transforming growth factor-beta], and MAPK), supported by increased α-SMA (alpha-smooth muscle actin), COL1 (collagen I), and TGF-β1 immunostaining, while metabolomics suggested perturbations in lipid metabolism and mitochondrial function. In mice, polystyrene exposure exacerbated isoprenaline-induced systolic dysfunction and myocardial fibrosis in both experimental paradigms and recapitulated pathway signatures related to cell-matrix interactions.CONCLUSIONSMyocardial MNP burden, particularly nanoplastics, is associated with greater fibrosis in humans, and experimental polystyrene exposure aggravates stress-induced myocardial remodeling in vivo. Multiomics analyses nominate inflammatory, ECM (extracellular matrix), and metabolic programs as candidate mediators of MNP-associated cardiotoxicity.","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"21 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147751383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.","authors":"Maartje Westhoff, Taylor L Voelker, Silvia G Del Villar, Phung N Thai, Hannah M Voorhees, Fatin Fazrina Roslan, Jody L Martin, Julie Bossuyt, Padmini Sirish, Nipavan Chiamvimonvat, Madeline Nieves-Cintrón, Eamonn J Dickson, Rose E Dixon","doi":"10.1161/CIRCRESAHA.125.327896","DOIUrl":"10.1161/CIRCRESAHA.125.327896","url":null,"abstract":"<p><strong>Background: </strong>Contractile dysfunction, hypertrophy, and cell death during heart failure are linked to altered Ca<sup>2+</sup> handling and elevated levels of the hormone AngII (angiotensin II), which signals through G<sub>q</sub> (Guanine nucleotide-binding protein alpha subunit q)-coupled AT<sub>1</sub>Rs (AngII type 1 receptors), initiating hydrolysis of phosphatidylinositol (4,5)-bisphosphate. Chronic elevation of AngII contributes to cardiac pathology, but the mechanisms linking sustained AngII signaling to heart dysfunction remain incompletely understood. Here, we demonstrate that chronic AngII exposure profoundly disrupts cardiac phosphoinositide homeostasis, triggering a cascade of cellular adaptations that ultimately impair cardiac function.</p><p><strong>Methods: </strong>Mice received 1-week infusions of AngII, bisperoxovanadium (1,10 phenanthroline), both, or saline via osmotic minipumps. We used mass spectrometry, super-resolution microscopy, electrophysiology, confocal imaging, immunoblot, echocardiography, and histology to assess phosphoinositide levels, L-type voltage-gated calcium channel Ca<sub>V</sub>1.2 localization, Ca<sup>2+</sup> handling, protein phosphorylation, cardiac function, and fibrosis.</p><p><strong>Results: </strong>Chronic AngII infusion caused widespread phosphoinositide imbalance, reducing phosphatidylinositol, phosphatidylinositol phosphate, phosphatidylinositol bisphosphate, and phosphatidylinositol (3,4,5)-trisphosphate levels. Ca<sub>V</sub>1.2 channels were partially redistributed from t-tubules to endosomal compartments. Despite reduced sarcolemmal channel expression, Ca<sup>2+</sup> currents and transients were maintained through enhanced PKA (protein kinase A)-mediated and CaMKII (Ca<sup>2+</sup>/calmodulin-dependent protein kinase II)-mediated phosphorylation of Ca<sup>2+</sup>-handling proteins. However, this compensation proved insufficient as cardiac function progressively declined, marked by pathological hypertrophy, t-tubule disruption, and diastolic dysfunction. PTEN (phosphatase and tensin homolog) inhibition preserved Akt signaling and protected against cardiac dysfunction and fibrosis without preventing cellular remodeling or altered calcium handling.</p><p><strong>Conclusions: </strong>These findings reveal a complex interplay between phosphoinositide signaling, ion channel trafficking, and compensatory phospho-regulation in AngII-induced cardiac pathology. We establish phosphatidylinositol (3,4,5)-trisphosphate depletion as a critical link between chronic AngII signaling and cardiac dysfunction. The dissociation between persistent cellular remodeling and preserved organ function with PTEN inhibition reveals that cardioprotection occurs primarily through reduced fibrosis. PTEN inhibition, thus, emerges as a promising therapeutic strategy for heart failure associated with pathological renin-angiotensin system activation, with potential to complement existing therapies by targ","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"e327896"},"PeriodicalIF":16.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13055796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147484875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension-Associated Acetate Deficiency Enhances Platelet Activation and Thrombosis Via Olfr78.","authors":"Yufei Chen, Biling Li, Yuan Lin, Wanmin Sha, Chenchen Shi, Mingzhu Wang, Shufang Wang, Jiaorui Wang, Yongbo Ma, Meiling Wu, Zhichao Fan, Yunfeng Chen, Yangfan Zhou, Deyu Fu, Jian Li, Yuejuan Zheng, Liang Hu","doi":"10.1161/CIRCRESAHA.125.327498","DOIUrl":"10.1161/CIRCRESAHA.125.327498","url":null,"abstract":"<p><strong>Background: </strong>Arterial thrombotic events constitute the leading cause of mortality in hypertension. Gut dysbiosis induces endothelial dysfunction and systemic inflammation, contributing to hypertension and its associated cardiovascular complications. Whether these dysbiotic microbiota metabolites in hypertension directly regulate platelet hyperactivation and thrombosis remains unclear.</p><p><strong>Methods: </strong>Fecal microbiota transplantation, 16S rRNA sequencing, and untargeted metabolomics were performed using samples from patients with hypertension. In vivo FeCl₃-induced mesenteric arteriole thrombosis model, ex vivo microfluidic whole-blood perfusion assay, and in vitro platelet functional studies defined the functional effects of acetate on platelet activation. Moreover, platelet-specific Olfr78 (olfactory receptor 78)-deficient mice were employed to explore the underlying mechanisms of acetate on platelet activation.</p><p><strong>Results: </strong>Transplantation with fecal microbiota from patients with hypertension enhanced in vivo FeCl₃-injured mesenteric arteriole thrombosis and ex vivo whole blood thrombus formation compared with fecal microbiota from healthy normotensive subjects. Untargeted metabolomics revealed that gut microbiota-derived acetate was decreased in patients with hypertension, and plasma acetate concentration negatively correlated with integrin αIIbβ3 activation and P-selectin exposure. Acetate demonstrated superior antiplatelet efficacy against ADP-induced aggregation, dense-granule secretion, α-granule secretion, and integrin αIIbβ3 activation than collagen or thrombin-induced platelet activation. Mechanistic studies using platelet-specific Olfr78^-/- mice revealed that acetate bound to and activated Olfr78, a receptor not previously reported to be expressed in platelets, to elevate cAMP level and activate PKA, thereby increasing p-VASP and decreasing Ca²⁺ mobilization as well as inactivating RhoA/ROCK2/MLC (myosin light chain) signaling to inhibit platelet activation. A high-fiber diet upregulated acetate/Olfr78 signaling in platelets to suppress microvascular thrombosis and protect against myocardial injury during myocardial infarction in mice.</p><p><strong>Conclusions: </strong>Acetate is a negative regulator of platelet hyperreactivity and thrombus formation via the Olfr78 receptor, and acetate deficiency contributes to platelet hyperreactivity in hypertension. Lifestyle modifications, particularly high-fiber dietary intervention and acetate supplementation, exhibit potent antithrombotic effects in hypertension.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"e327498"},"PeriodicalIF":16.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interleukin 11-Induced MicroRNAs as Functional Mediators and Circulating Biomarkers of Cardiac Fibrosis.","authors":"Roman Tikhomirov, Veronika Boichenko, Benedict Reilly-O'Donnell, Carla Lucarelli, Prashant Kumar Srivastava, Maryam Anwar, Chi Him Kendrick Yiu, Julia Dielesen, Victoria Maria Noakes, Santiago Nicolas Piella, Diana Kazharova, Mathilde Labbé, Zoe Kwan, Germana Zaccagnini, Catherine Mansfield, Maddalena Tessari, Lorenzo Menicanti, Simona Greco, Mark Sweeney, Joseph Okafor, Przemysław Leszek, Giuseppe Faggian, Giovanni Battista Luciani, Costanza Emanueli, Fabio Martelli, Julia Gorelik","doi":"10.1161/CIRCRESAHA.125.326799","DOIUrl":"10.1161/CIRCRESAHA.125.326799","url":null,"abstract":"<p><strong>Background: </strong>Cardiac fibrosis can be triggered by several pathologies, including ischemic heart disease and aortic stenosis. Cardiac fibrosis is brought about by uncontrolled ECM (extracellular matrix) deposition by myofibroblasts. IL (interleukin)-11 (<i>Il11</i>) has been demonstrated as a trigger of multiorgan fibrosis. However, the molecular mechanisms underpinning IL-11-induced fibrosis require further characterization. Recent studies indicate that microRNA dysregulation contributes to the pathogenesis of cardiac fibrosis and can be targeted therapeutically. This study explored the hypothesis that microRNAs act as downstream effectors of IL-11-induced cardiac fibrosis. Moreover, we investigated the translational potential of IL-11-regulated microRNAs as circulating biomarkers of cardiac fibrosis in patients with aortic stenosis.</p><p><strong>Methods: </strong>A bioinformatic microRNA target prediction analysis was used to identify candidate microRNAs regulated by IL-11. Experimental validation was performed in cardiac fibroblasts from postinfarction failing and healthy rat hearts, after IL-11 stimulation. Functional studies assessed the effects of microRNA modulation on fibrotic gene expression in cardiac fibroblasts using microRNA inhibitor-based and mimic-based transfection. Bioinformatic analysis and luciferase assay identified candidate microRNA targets downstream of IL-11. Findings were further evaluated in transverse aortic constriction and cardiomyocyte-specific <i>Il11</i>-overexpression (Tg-Il11 [transgenic mouse model with cardiomyocyte-specific <i>Il11</i> overexpression]) mouse models and in left ventricular tissue, peripheral plasma, and plasma extracellular vesicles from patients with aortic stenosis.</p><p><strong>Results: </strong>MicroRNA-27b-5p and microRNA-497-5p were identified as novel downstream effectors of IL-11 signaling. IL-11 increased the expression of both microRNAs in cardiac fibroblasts; transfection with either microRNA inhibitor reduced, whereas microRNA mimics increased, profibrotic mRNA levels. Furthermore, microRNA-27b-5p and microRNA-497-5p converged on HIF (hypoxia-inducible factor)-1 signaling by targeting its regulator EGLN (Egl-9 family hypoxia-inducible factor). Increased microRNA levels were observed alongside reduced expression of Egln1 and Egln2 in 2 mouse models. In patients with aortic stenosis, myocardial and circulating levels of these microRNAs correlated with the severity of left ventricular fibrosis, indicating these microRNAs' potential as new circulating biomarkers of cardiac fibrosis.</p><p><strong>Conclusions: </strong>In this study, we have newly identified the potential value of microRNA-27b-5p and microRNA-497-5p as actionable biomarkers of the profibrotic response to IL-11 in the heart. Future studies should validate the translational potential of the microRNAs as new clinical biomarkers and therapeutic targets.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"e326799"},"PeriodicalIF":16.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13108434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium Channel Isoform Diversity Underlies Chamber-Specific Cardiac Excitability.","authors":"Colin J Clark, Christian E Anderson, Alex Dou, Jason M Dierdorff, Jason D Galpin, Lionel Gissot, Samantha G Thompson, Hannah Choi, Jin-Young Yoon, Daniel T Infield, Jared M McLendon, Jasmyn M Hoeger, Omar Rabab'h, Peter Bronk, Keane Leeds, William J Kutschke, William J Paradee, Ryan L Boudreau, Bum-Rak Choi, Barry London, Christopher A Ahern","doi":"10.1161/CIRCRESAHA.125.328159","DOIUrl":"10.1161/CIRCRESAHA.125.328159","url":null,"abstract":"<p><strong>Background: </strong>Na_V (voltage-gated sodium) channels drive cardiac excitability. Although Na_V1.5 is the primary cardiac isoform, the composition and functional contributions of non-Na_V1.5 isoforms in the heart remain unclear.</p><p><strong>Methods: </strong>Here, we developed a chemical-genetic mouse model (Na_V1.5^GX/GX) in which Na_V1.5 can be selectively and reversibly inhibited by acyl- and aryl-sulfonamide compounds (GX [acyl- and aryl-sulfonamide compounds typically denoted by the name GX-### and associated items] drugs). Cardiac activity was assessed by electrocardiograms in vivo, and optical mapping was used for imaging of ex vivo hearts. Whole-cell voltage-clamp in tandem with validated toxins and isoform-selective inhibitors were used to examine sodium current composition.</p><p><strong>Results: </strong>Na_V1.5^GX/GX mice exhibited normal cardiac function at baseline, but acute GX drug administration caused profound conduction defects and arrhythmias. Whole-heart optical mapping revealed dose-dependent chamber-specific sensitivity to Na_V1.5 inhibition, with the right ventricle being the most sensitive, followed by the left ventricle, left atrium, and right atrium. Patch-clamp recordings of isolated cardiomyocytes with application of Na_V isoform-selective inhibitors showed that Na_V1.5 contributed 93% of sodium current in the left ventricle, 79% in the right ventricle, and 78% in the atria. Non-Na_V1.5 isoforms were differentially enriched across chambers: Na_V1.8 in the left ventricle, Na_V1.1/1.3 in the right ventricle, and Na_V1.2/1.6/1.7 in the atria.</p><p><strong>Conclusions: </strong>These results reveal a surprising chamber-specific isoform landscape of cardiac sodium currents, which may underlie the right ventricular predominant phenotype of Brugada syndrome. These data highlight non-Na_V1.5 isoforms as potential mediators of chamber-specific cardiac pathologies and as pharmacological targets.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"e328159"},"PeriodicalIF":16.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13045664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meet the First Authors.","authors":"","doi":"10.1161/RES.0000000000000752","DOIUrl":"https://doi.org/10.1161/RES.0000000000000752","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"138 9","pages":"e000752"},"PeriodicalIF":16.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular Endothelial Growth Factor-D Improves Lung Vascular Integrity During Acute Lung Injury.","authors":"Yongdae Yoon, Lokesh Sharma, Wenwen Tang, Shannon Kirk, Micha Sam Brickman Raredon, Farida Ahangari, Johad Khoury, Hong Qian, Yunbo Ke, Mohan E Tulapurkar, Ruya Liu, Yi Luan, Qianying Yuan, Lujia Chen, Konstantin G Birukov, Michael Simons, Dianqing Wu, Laura E Niklason, Naftali Kaminski, Yifan Yuan","doi":"10.1161/CIRCRESAHA.124.326094","DOIUrl":"10.1161/CIRCRESAHA.124.326094","url":null,"abstract":"<p><strong>Background: </strong>Disorders in pulmonary vascular integrity are a prominent feature in many lung diseases. Paracrine signaling is highly enriched in the lung and plays a crucial role in regulating vascular homeostasis. However, the specific local cell-cell crosstalk signals that maintain pulmonary microvascular stability in adult animals and humans remain largely unexplored.</p><p><strong>Methods: </strong>In this study, we used single-cell RNA-sequencing-based computational pipelines to systematically profile ligand-receptor interactions within the lung microvascular niche and identified VEGF-D (vascular endothelial growth factor-D) as a key local factor with previously unrecognized barrier-protective properties in models of acute lung injury.</p><p><strong>Results: </strong>Our single-cell RNA-sequencing data revealed that, under physiological conditions, soluble ligand-receptor interactions between mesenchymal cells, in particular alveolar fibroblasts, and microvascular endothelial cells are predominantly associated with pathways involved in maintaining vascular integrity as compared with all other cells. On treatment with top identified ligands, we found that VEGF-D significantly enhanced endothelial barrier function and conferred protection against inflammatory challenges induced by TNF-α (tumor necrosis factor-α), IL (interleukin)-1β, and thrombin. This barrier-protective effect of VEGF-D was significantly attenuated by inhibition of VEGFR2 (vascular endothelial growth factor receptor 2), either through small interfering RNA (siRNA) knockdown or pharmacological blockade using specific VEGFR2 inhibitors. Intravenous administration of recombinant VEGF-D in lipopolysaccharide-induced acute lung injury models significantly reduced vascular permeability (7339±2510 arbitrary unit [a.u.] [lipopolysaccharides] versus 5350±1821 a.u. [lipopolysaccharides+VEGF-D]; <i>P</i><0.05), immune cell infiltration (0.791±0.199×10⁶ whole blood cells/mL [lipopolysaccharides] versus 0.540±0.190×10⁶ whole blood cells/mL [lipopolysaccharide+VEGF-D]; <i>P</i><0.01), and the expression of proinflammatory markers TNF-α, IL-6, and keratinocyte chemoattractant in the lung tissue. This effect was abolished in <i>VEGFR2</i>^<i>iECKO</i> (VEGFR2 inducible endothelial cells knockout) mice, confirming that VEGF-D mediates its effects via VEGFR2-dependent signaling.</p><p><strong>Conclusions: </strong>This study demonstrates an unexpected protective role for VEGF-D in promoting lung endothelial barrier integrity and suggests that paracrine signaling from the alveolar fibroblast niche contributes critically to lung capillary homeostasis.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"e326094"},"PeriodicalIF":16.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13007730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac Sodium Channel Regulation: A Potential New Therapeutic Target in Cardiomyopathy.","authors":"Samuel C Dudley","doi":"10.1161/circresaha.126.328285","DOIUrl":"https://doi.org/10.1161/circresaha.126.328285","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"48 1","pages":"e328285"},"PeriodicalIF":20.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147735493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Love Thy Neighbor: A Fibroblast-to-Endothelial Niche That Improves Lung Injury.","authors":"Akito Eguchi,Jonathan D Brown","doi":"10.1161/circresaha.126.328510","DOIUrl":"https://doi.org/10.1161/circresaha.126.328510","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"29 1","pages":"e328510"},"PeriodicalIF":20.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147735492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphoinositides in Chronic Ang II Signaling: PTEN-A Target in Heart Failure?","authors":"Constanze Schanbacher,Kristina Lorenz","doi":"10.1161/circresaha.126.328513","DOIUrl":"https://doi.org/10.1161/circresaha.126.328513","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"45 1","pages":"e328513"},"PeriodicalIF":20.1,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147735494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}