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  • 1
    Online Resource
    Online Resource
    Abstract P157: Tractography of White Matter Connections Predicts for Vascular Cognitive Impairment in Hypertensive Patients
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Hypertension Vol. 66, No. suppl_1 ( 2015-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 66, No. suppl_1 ( 2015-09)
    Abstract: Vascular cognitive impairment (VCI) results by several vascular risk factors and, particularly, hypertension (HTN). The identification of early changes associated with later development of dementia is demanding. Great part of research has primarily focused on brain changes occuring in grey matter. However, more recent data highlighted that HTN may determine cognitive decline, even before manifest neurodegeneration. Diffusion tensor imaging (DTI) on magnetic resonance, opened the possibility to predict white matter connections that correlate with specific cognitive functions. In this study, we used DTI and cognitive assessment (CA), in order to identify a regional pattern of fractional anisotropy (FA) changes that could predict for VCI in hypertensive patients (HT). We have examined 15 HT (moderate to severe, with antihypertensive medications) vs 15 normotensive (NT), subjecting them to DTI and CA. HT had significant higher SBP (138±4 vs 118±3 in NT) and DBP (87±2 vs 75±2 in NT) (p 〈 0.001), displayed a significant LV hypertrophic remodeling (LVM/BSA 112±5 vs 83±3 for NT) (p 〈 0.0001), with a significant moderate increase in albuminuria (15.7±2.6 mg/24h vs 8.8±1.6 for NT) (p 〈 0.03). When subjected to CA, HT had significantly worsen performance on both MoCA (22.66±0.97 vs 26.21±0.57 NT) and Stroop Test (34.50±3.87 vs 17.75±2.57 NT) (p 〈 0.01). Conversely, tests regarding Verbal Fluency and Instrumental Activities of Daily Living revealed normal performance of HT, thus indicating a selective impairment of memory. Brain imaging showed that, while none of the patients had abnormal signal intensity on T1/T2-weighted MRI, DTI indices FA were significantly reduced in HT as vs NT. In particular, HT had lower FA in projection fibers related to impairment for non-verbal materials (Anterior Thalamic Radiation: 0.358±0.012 vs 0.330±0.006, p 〈 0.05), association fibers involved in executive functioning and emotional regulation (Superior Longitudinal Fasciculus: 0.388±0.013 vs 0.356±0.007, p 〈 0.05), limbic system fibers involved in attention tasks (cingulate gyrus: 0.364±0.009 vs 0.328±0.010, p 〈 0.01). Our data highlight a novel paradigm of combined DTI/CA of HT patients, capable to identify, with great sensitivity, predictive signs of HTN-induced VCI.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.66.suppl_1.p157
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    Abstract 132: Obesity-Related Hypertension Develops Through Splenic Sympathetic Overactivity and is Mediated by Immune-Modulating Functions of Placental Growth Factor
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Hypertension Vol. 72, No. Suppl_1 ( 2018-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 72, No. Suppl_1 ( 2018-09)
    Abstract: Obesity-related hypertension (HTN) is an epidemic health problem and a major risk factor for the development of cardiovascular disease. A consistent amount of research on the pathophysiological basis of obesity has implicated a crucial role of sympathetic overdrive. Interestingly, an overactivation of the sympathetic nervous system (SNS) accompanies HTN as well. Recent data highlighted that increased SNS activation in HTN is important in modulating immune responses, besides controlling typical cardiovascular functions. Whether neuroimmune mechanisms are relevant in obesity-induced HTN is still unknown. To test this hypothesis we subjected 6 week-old C57Bl/6J mice to high fat diet (HFD), as compared to low fat diet (LFD) and monitored blood pressure (BP), which started to rise after 2 months and steadily increased up to 4 months. We measured circulating noradrenalin, finding it significantly elevated 2 months after HFD. To gain insights in the potential SNS modulation of immunity, we measured by microneurography SNS activation on the splenic nerve. Firing frequency (FF, spikes in 10') of splenic nerve was increased in C57Bl/6J mice on HFD (FF:432±81) as compared to LFD (FF:86±10, p 〈 0.01). Then, we surgically removed splenic innervation by left celiac ganglionectomy (CGX) and fed mice with HFD for 4 months. Despite CGX-mice become obese similarly to sham, as shown by body weight and microCT-measured fat pad, they were protected from HTN (SBP mmHg =CGX:105±4; sham:125±5, p 〈 0.001), suggesting that the splenic sympathetic overdrive influences BP responses but not metabolic alterations. To look for molecular determinants, we analyzed the expression of Placental Growth Factor (PlGF), previously identified as a neuroimmune mediator, and found it significantly increased in the spleen upon HFD, but only with intact SNS innervation, since CGX-mice did not increase it. In the end, PlGF KO mice subjected to HFD, although becoming obese as much as WT, were protected from HTN (SBP mmHg =PlGF KO:103±4; WT:123±6, p 〈 0.001). Interestingly, both CGX and PlGF KO mice displayed a reduced egression of activated T cells from the spleen upon HFD feeding, suggesting that the protection observed could be related to reduced infiltration of activated lymphocytes in target organs.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.72.suppl_1.132
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2094210-2
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  • 3
    Online Resource
    Online Resource
    Abstract 14024: High-Field MRI Advanced Neuroimaging Characterization of Cerebrovascular Damage in a Mouse Model of Hypertension-Induced Cognitive Impairment
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: Hypertension in one of the main risk factors for vascular cognitive impairment (VCI) and neurodegenerative pathologies as Alzheimer’s Disease (AD). To identify the underlying mechanisms it is important to use experimental models that present the pathophysiological characteristics of AD and VCI, hence allowing the investigation of molecular processes not explorable in humans. To ease the translational potential of these findings it is fundamental to characterize the brain damage with techniques easily applicable to the cognitive-declining patient, like MRI. Methods: Transverse aortic constriction (TAC) was performed in C57Bl/6J mice to induce severe hypertension to the cerebral vasculature and long term VCI. The cognitive performance at the Morris Water Maze (MWM) and Novel Object Recognition (NOR), the cerebrovascular injury by macro and microstructural MRI and cerebral blood flow (CBF) were analyzed. T2w volumetric images, diffusion tensor imaging, CBF sequences were performed on a small-animal dedicated 7 Tesla MRI. Results: TAC-hypertensive mice displayed significantly reduced learning capabilities, evidenced in the acquisition phase of MWM, and a marked impairment in spatial and short-term memory shown by probe trial in MWM and NOR test. At the structural MRI, TAC mice showed white matter microstructural degradation in the Fimbria, evidenced by a reduction of Fractional Anisotropy (SHAM vs TAC: 0.52±0.01 vs 0.44±0.02, p=0.047), coupled with a hypothalamic swelling (Right: SHAM vs TAC: 7.14±0.09 vs 7.50±0.11mm 3 , p=0.035; Left: SHAM vs TAC: 7.18±0.20 vs 7.91±0.17mm 3 , p=0.019). Hemodynamic alterations resulted in reduced cortical and hypothalamic CBF (Cortex: SHAM vs TAC: 96.6±3.4 vs 77.1±6.8 mL/100mg/min, p=0.046; Hypothalamus: SHAM vs TAC: 140±6 vs 122±4 mL/100mg/min, p=0.025). Furthermore the histological analysis evidenced a capillary rarefaction and reduced capillary-pericyte coverage in the prefrontal cortex, suggestive of a severe impact of the elevated blood pressure on the brain vasculature. Conclusions: In conclusion we have developed a mouse model of hypertension that reproduces typical tracts of the human pathology and a pipeline of analysis that will ease translate findings from bench to bedside.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.14024
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Abstract 300: Targeting IL-1β Protects From Aortic Aneurysms Induced by Disrupted TGFβ signaling in SMCs
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 37, No. suppl_1 ( 2017-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. suppl_1 ( 2017-05)
    Abstract: Aortic aneurysms represent a life-threatening condition because of the current lack of effective treatment, with therapeutic options limited to emergency surgery. Aneurysm formation is typically associated with extracellular matrix remodeling and persistent inflammation. Although the molecular mechanisms underlying aortic pathology remain largely unclear, TGFβ signaling is unquestionably implied and its downstream target Smad4 showed protective functions for maintenance of aortic walls’ integrity. Using mice with smooth muscle cells (SMCs) specific deletion of Smad4 in the adult ( Smad4 -SMC iko ), developing spontaneous aneurysms, we investigated the molecular mechanisms activated by dysregulation of TGFβ signaling. Structural disarrangement of ascending aorta media in Smad4 -SMC iko mice was clearly appreciated early after Smad4 deletion as discrete breaks of elastic lamellae. Interestingly, the islands of damage evidenced in the aorta of Smad4 -SMC iko were enriched of immune infiltrate, mainly composed by monocytes/macrophages, as indicated by flow cytometry and immunofluorescence. We then analyzed several pathways downstream to Smad4 inhibition, finding a selective activation of NF-kB/IL-1β pathway in SMCs. This danger signal released by SMCs later recruits innate immunity, hence arising inflammation. In order to test the relevance of this pathway in the formation of aneurysms induced by TGFβ dysregulation, we deleted Smad4 in SMCs of mice with Il1r1 null background ( Smad4 -SMC iko ; Il1r1 -/- ). Serial ultrasonographic analyses revealed that ablation of IL1 receptor 1 protected mice with the SMCs deletion of Smad4 from the progression of pathology and improved their overall survival. In the end, to test the translational potential of our findings, we neutralized IL-1β signaling with the clinically relevant murine version of the FDA-approved clinical drug canakinumab. During a time course of 16 weeks, while a weekly administration of control immunoglobulins did not change aneurysm progression in Smad4 -SMC iko mice, treatment with anti-IL-1β antibody significantly hampered aneurysm formation in the aorta. These findings identify a mechanistic target for controlling aneurysms progression induced by disrupted TGFβ signaling.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.37.suppl_1.300
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1494427-3
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  • 5
    Online Resource
    Online Resource
    Abstract 15180: Cerebral Blood Flow Measured by Mri is a Key Translational Hallmark of Brain Injury in Experimental Models of Hypertension-Induced Cognitive Impairment
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: While several works pointed out the epidemiological associations between hypertension and dementia, the underlying mechanisms are still relatively unknown. In this work we focused on the application of translational tools like MRI to investigate the brain injury induced by hypertension and characterized by cognitive impairment and neuroinflammation. Cerebral hypertension was induced in mice by transverse aortic constriction (TAC) or sham procedure, as previously demonstrated by our group. We characterized cerebral blood flow (CBF) by 7T MRI, measuring the cerebral tissue blood prefusion. Morris Water Maze (MWM) was used to evaluate cognitive function in hypertensive and normotensive mice. Cortical microvasculature was analyzed in histological brain sections. A group of mice was treated with an antibody neutralizing IFNy, a key proinflammatory cytokine induced by hypertension. TAC mice showed a marked cerebral hypoperfusion, with CBF reduction in cortex (Sham: 96.58 vs TAC: 74.25 mL/100g/min p=0.024) and hypothalamus (Sham: 140 vs TAC: 121.4 mL/100g/min p=0.027). Tissue analysis revealed a reduction in capillary density defined as portion of field of view (FOV) occupied by capillaries (Sham: 11.3% vs TAC: 7.7%, p=0.004) and loss of their integrity in the cortex of hypertensive mice, defined as pericyte coverage percentage in the FOV (Sham: 79% vs TAC: 36%, p=0.01). Finally, the impairment in cognitive function measured by the MWM correlated with the CBF measures (r 2 :0.407, p=0.01). In the end, we subjected TAC mice to anti-IFNy treatment and analyzed the effects on brain vasculature assessed in vivo by MRI and ex vivo by histology. We observed that, while leaving unchanged the hemodynamic challenge on the brain, the treatment induced a global rescue in CBF (TAC: 99.85 vs TAC anti-IFNy: 116 mL/100g/min p=0. 008) and a strong correlation between MRI-measured CBF and microvascular density (r 2 :0.471, p=0.002). In conclusion, CBF evaluated by MRI is a key translational hallmark of hypertensive brain injury, and its evaluation in the clinical setting can provide insights on cerebral microvasculature health.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.15180
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 6
    Online Resource
    Online Resource
    Abstract P511: Targeting Il-1β Protects From Aortic Aneurysms Induced by Disrupted Tgfβ Signaling in Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Hypertension Vol. 70, No. suppl_1 ( 2017-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 70, No. suppl_1 ( 2017-09)
    Abstract: Aortic aneurysms represent a life-threatening condition because of the current lack of effective treatments. Aneurysm formation is typically associated with extracellular matrix remodeling and persistent inflammation. Although the molecular mechanisms underlying aortic pathology remain largely unclear, TGFβ signaling is unquestionably implied and its downstream target Smad4 showed protective functions for maintenance of aortic walls’ integrity. Using mice with smooth muscle cells (SMCs) specific deletion of Smad4 in the adult ( Smad4 -SMC iko ), developing spontaneous aneurysms (Ascending Aorta Diameter: Smad4 -SMC iko 2.15±0.03; Smad4 -SMC wt 1.7±0.03;***p 〈 0.001), we investigated the molecular mechanisms activated by dysregulation of TGFβ signaling. Structural disarrangement of ascending aorta in Smad4 -SMC iko mice was clearly appreciated early after Smad4 deletion as discrete breaks of elastic lamellae (breaks/section: Smad4 -SMC iko 2.05±0.5; Smad4 -SMC wt 0.83±0.4;***p 〈 0.001). Interestingly, the islands of damage in the aorta of Smad4 -SMC iko were enriched of immune infiltrate, mainly monocytes/macrophages, as indicated by FACS and immunofluorescence. We then analyzed several pathways downstream to Smad4 inhibition, finding a selective activation of NF-kB/IL-1β in SMCs. To test the relevance of this pathway in the formation of aneurysms, we deleted Smad4 in SMCs of mice with Il1r1 null background ( Smad4 -SMC iko ; Il1r1 -/- ). Ultrasonographic analyses revealed that ablation of IL1 receptor1 protected Smad4 -SMC iko mice from the progression of pathology and improved their overall survival. In the end, to test the translational potential of our findings, we neutralized IL-1β signaling with the clinically relevant murine version of the FDA-approved clinical drug canakinumab. During a time course of 16 weeks, while a weekly administration of control immunoglobulins did not change aneurysm progression in Smad4 -SMC iko mice, treatment with anti-IL-1β antibody significantly hampered aneurysm formation in the aorta ( Smad4 -SMC iko +anti- IL-1β 1.85±0.02; Smad4 -SMC iko +anti-IgG 2.09±0.03; ***p 〈 0.001) These findings identify a mechanistic target for controlling aneurysms progression induced by disrupted TGFβ signaling.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.70.suppl_1.p511
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2094210-2
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  • 7
    Online Resource
    Online Resource
    Abstract 094: Adaptive Cardiac Remodeling to Chronic Pressure Overload Requires the Expression of Placental Growth Factor in the Spleen to Recruit Reparative Macrophages to the Left Ventricle
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Hypertension Vol. 74, No. Suppl_1 ( 2019-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 74, No. Suppl_1 ( 2019-09)
    Abstract: Cardiac remodeling is the process established by the left ventricle (LV) to respond to different challenging stimuli. Although immunity has been clearly shown to participate to LV remodeling in myocardial infarction, how immune response participates to hypertensive chronic stress is poorly understood. We found that Placental Growth Factor (PlGF), belonging to the VEGF family, is necessary for adaptive remodeling to pressure overload and modulates the recruitment of innate immune cells in the LV. Here we asked where PlGF does exert its effects: i) directly in the myocardium or ii) by modulating immune organs? As TAC induced PlGF both in cardiac tissue and in the spleen, we devised a strategy to assess the contribution of these two tissues. We generated chimeric mice by spleen transplantation between WT and KO mice, obtaining: 1) WT mice with PlGF KO spleen and 2) PlGF KO mice with WT spleen (EF% 78 ± 0,7), finding that only mice with PlGF expressed in the spleen (EF% 68 ± 1,5) established adaptive remodeling to pressure overload, as assessed by echocardiography (p 〈 0.01). Since in the absence of PlGF we observed a consistent reduction of LV macrophages, we characterized the subsets of innate immune cells by flow cytometry. While WT mice subjected to TAC showed early LV recruitment of non resident CD11b + CD64 + Timd4 - CCR2 low CX 3 CR1 hi macrophages, PlGF KO mice failed to show this response. To investigate the potential relevance of the spleen as reservoir of myeloid cells with adaptive/reparative functions for LV, we induced TAC in splenectomized mice, finding that they didn’t develop adaptive remodeling, exhibiting early HFrEF. To investigate the role of reparative macrophages, that are mostly characterized by the expression of the CX 3 CR1 receptor, and of pro-inflammatory monocytes that express high levels and accumulate through CCR2, we also subjected CCR2 KO and CX 3 CR1 KO mice to TAC. While CCR2 KO behaved similarly to WT mice, CX 3 CR1 KO were unable to establish adaptive remodeling and early developed HFrEF similarly to mice deprived of the spleen and to PlGF KO mice. Overall our results indicate that pressure overload induces PlGF in the spleen as an immunomodulator capable to deploy reparative macrophages that sustain adaptive remodeling of the LV.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.74.suppl_1.094
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2094210-2
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  • 8
    Online Resource
    Online Resource
    PS-B10-10: MRI CEREBROVASCULAR CHARACTERIZATION IN A MOUSE MODEL OF HYPERTENSION-INDUCED BRAIN INJURY
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Journal of Hypertension Vol. 41, No. Suppl 1 ( 2023-01), p. e448-
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. Suppl 1 ( 2023-01), p. e448-
    Type of Medium: Online Resource
    ISSN: 0263-6352 , 1473-5598
    URL: Article
    DOI: 10.1097/01.hjh.0000917444.34124.34
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2017684-3
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  • 9
    Online Resource
    Online Resource
    Interferon-γ drives macrophage reprogramming, cerebrovascular remodelling, and cognitive dysfunction in a zebrafish and a mouse model of ion imbalance and pressure overload
    Oxford University Press (OUP) ; 2023
    In:  Cardiovascular Research Vol. 119, No. 5 ( 2023-05-22), p. 1234-1249
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 119, No. 5 ( 2023-05-22), p. 1234-1249
    Abstract: Dysregulated immune response contributes to inefficiency of treatment strategies to control hypertension and reduce the risk of end-organ damage. Uncovering the immune pathways driving the transition from the onset of hypertensive stimulus to the manifestation of multi-organ dysfunction are much-needed insights for immune targeted therapy. Methods and results To aid visualization of cellular events orchestrating multi-organ pathogenesis, we modelled hypertensive cardiovascular remodelling in zebrafish. Zebrafish larvae exposed to ion-poor environment exhibited rapid angiotensinogen up-regulation, followed by manifestation of arterial hypertension and cardiac remodelling that recapitulates key characteristics of incipient heart failure with preserved ejection fraction. In the brain, time-lapse imaging revealed the occurrence of cerebrovascular regression through endothelial retraction and migration in response to the ion-poor treatment. This phenomenon is associated with macrophage/microglia-endothelial contacts and endothelial junctional retraction. Cytokine and transcriptomic profiling identified systemic up-regulation of interferon-γ and interleukin 1β and revealed altered macrophage/microglia transcriptional programme characterized by suppression of innate immunity and vasculo/neuroprotective gene expression. Both zebrafish and a murine model of pressure overload-induced brain damage demonstrated that the brain pathology and macrophage/microglia phenotypic alteration are dependent on interferon-γ signalling. In zebrafish, interferon-γ receptor 1 mutation prevents cerebrovascular remodelling and dysregulation of macrophage/microglia transcriptomic profile. Supplementation of bone morphogenetic protein 5 identified from the transcriptomic approach as a down-regulated gene in ion-poor-treated macrophages/microglia that is rescued by interferon-γ blockage, mitigated cerebral microvessel loss. In mice subjected to transverse aortic constriction-induced pressure overload, typically developing cerebrovascular injury, neuroinflammation, and cognitive dysfunction, interferon-γ neutralization protected them from blood–brain barrier disruption, cerebrovascular rarefaction, and cognitive decline. Conclusions These findings uncover cellular and molecular players of an immune pathway communicating hypertensive stimulus to structural and functional remodelling of the brain and identify anti-interferon-γ treatment as a promising intervention strategy capable of preventing pressure overload-induced damage of the cerebrovascular and nervous systems.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvac188
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1499917-1
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  • 10
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    Online Resource
    Targeting Interleukin-1β Protects from Aortic Aneurysms Induced by Disrupted Transforming Growth Factor β Signaling
    Elsevier BV ; 2017
    In:  Immunity Vol. 47, No. 5 ( 2017-11), p. 959-973.e9
    Details
    In: Immunity, Elsevier BV, Vol. 47, No. 5 ( 2017-11), p. 959-973.e9
    Type of Medium: Online Resource
    ISSN: 1074-7613
    URL: Article
    DOI: 10.1016/j.immuni.2017.10.016
    RVK:
    XA 48754.8
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 2001966-X
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