3 research outputs found
A bibliometric analysis of the 100 top-cited systematic review and meta-analysis in Orthodontics
No full textABSTRACT Objective: This bibliometric study aimed to analyze the citation metrics, journal and author characteristics, and subject domains of the 100 top-cited Systematic Reviews (SR) and Meta-Analysis (MA) in orthodontics. Material and Methods: An electronic database search was conducted for SR and MA in the Web of Science on 16th July 2023, without language and time restrictions. Of the 802 hits returned, the 100 top-cited orthodontic articles were shortlisted. They were analyzed for citation metrics, journal characteristics (journal, year of publication, impact factor-IF), author and affiliation characteristics (number, primary and corresponding author’s affiliation, and country), study domain, and keywords. Results: These articles were published from 1996 to 2021 in 20 journals, with an impact factor of 1.9 to 10.5, by 351 researchers affiliated with 104 universities. Their citations ranged from 45 to 344, and 34 poised to be classified as classic (≥ 100 citations). The maximum number of articles was published in the American Journal of Orthodontics and Dentofacial Orthopedics (n=38), the European Journal of Orthodontics (n=18), and the Angle Orthodontist (n=8). The authors for individual papers ranged from 1 to 10, with 5 being the most common (n=58). Europe had the highest contribution regarding the number of corresponding authors, institutions, and citations. Bone anchorage and orthodontic tooth movement/Biomechanics were the most frequently researched domains (n=11 each). The most common keyword used was Orthodontics (n=19), followed by Systematic Review (n=16) and Meta-analysis (n=9). Conclusion: In general, the top cited SR and MA were published in high-impact orthodontic journals, were multi-authored, and reflected the collaborative work from different universities
Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart
No full textAims Members of the VEGF family are crucial modulators of vascular and neural function. While VEGFA signalling has been shown to mitigate several aging-related cardiac phenotypes and prolong survival in aged mice, the role of VEGFB in cardiac aging remains underexplored. In this study, we identify a significant decline in Vegfb expression, particularly of its soluble isoform Vegfb186, in aged mouse and human hearts. To assess the therapeutic potential of VEGFB in aging-associated cardiac pathologies, we used AAV9-mediated gene transfer to overexpress Vegfb186 in 18-month-old male C57Bl/6J mice.Methods and results VEGFB is known to exhibit vascular and neuroprotective effects that we assessed in the ageing heart. In the aged heart, doses of Vegfb186 overexpression that had only a modest effect on the vascular endothelium prevented age-induced diastolic dysfunction and fibrosis. Vegfb186 treatment additionally restored sympathetic and sensory nerve fibre density and increased heart rate variability. Although Vegfb186 overexpression induced cardiac hypertrophy, our findings indicated that this hypertrophy was compensatory rather than pathological as Vegfb186 overexpression corrected the elevated cardiomyocyte length-to-width ratio observed in aged hearts, a metric typically indicative of pathological remodelling. Cardiac single-nucleus RNA sequencing of the hearts and in vitro analysis of the cardiomyocytes indicated up-regulation of the STAT3 signal transduction pathway as a potential contributor of VEGFB-induced cardiac hypertrophy.Conclusion Our findings demonstrate that Vegfb186 overexpression partially reverses age-related cardiac pathologies such as diastolic dysfunction and fibrosis. This work highlights VEGFB as a potential therapeutic target for combating cardiac aging and its associated dysfunctions.Peer reviewe
Aging impairs the neurovascular interface in the heart
No full textAging is a major risk factor for impaired cardiovascular health. Because the aging myocardium is characterized by microcirculatory dysfunction, and because nerves align with vessels, we assessed the impact of aging on the cardiac neurovascular interface. We report that aging reduces nerve density in the ventricle and dysregulates vascular-derived neuroregulatory genes. Aging down-regulates microRNA 145 (miR-145) and derepresses the neurorepulsive factor semaphorin-3A. miR-145 deletion, which increased Sema3a expression or endothelial Sema3a overexpression, reduced axon density, mimicking the aged-heart phenotype. Removal of senescent cells, which accumulated with chronological age in parallel to the decline in nerve density, rescued age-induced denervation, reversed Sema3a expression, preserved heart rate patterns, and reduced electrical instability. These data suggest that senescence-mediated regulation of nerve density contributes to age-associated cardiac dysfunction
