Vascular biology (Bristol, England)最新文献

{"title":"Cardiac revascularization: state of the art and perspectives.","authors":"Ambra Cappelletto,&nbsp;Serena Zacchigna","doi":"10.1530/VB-19-0011","DOIUrl":"https://doi.org/10.1530/VB-19-0011","url":null,"abstract":"<p><p>Cardiac ischemia is the leading cause of morbidity and mortality in a worldwide epidemic. The progressive understanding of the mechanisms driving new blood vessel formation has led to numerous attempts to revascularize the ischemic heart in animal models and in humans. Here, we provide an overview of the current state of the art and discuss the major obstacles that have so far limited the clinical success of cardiac revascularization.</p>","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"H47-H51"},"PeriodicalIF":0.0,"publicationDate":"2019-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38377220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pericytes in the infarcted heart.","authors":"Linda Alex,&nbsp;Nikolaos G Frangogiannis","doi":"10.1530/VB-19-0007","DOIUrl":"https://doi.org/10.1530/VB-19-0007","url":null,"abstract":"<p><p>The adult mammalian heart lacks regenerative capacity and heals through activation of an inflammatory cascade that leads to the formation of a collagen-based scar. Although scar formation is important to preserve the structural integrity of the ventricle, unrestrained inflammation and excessive fibrosis have been implicated in the pathogenesis of adverse post-infarction remodeling and heart failure. Interstitial cells play a crucial role in the regulation of cardiac repair. Although recent studies have explored the role of fibroblasts and immune cells, the cardiac pericytes have been largely ignored by investigators interested in myocardial biology. This review manuscript discusses the role of pericytes in the regulation of inflammation, fibrosis and angiogenesis following myocardial infarction. During the inflammatory phase of infarct healing, pericytes may regulate microvascular permeability and may play an important role in leukocyte trafficking. Moreover, pericyte activation through Toll-like receptor-mediated pathways may stimulate cytokine and chemokine synthesis. During the proliferative phase, pericytes may be involved in angiogenesis and fibrosis. To what extent pericyte to fibroblast conversion and pericyte-mediated growth factor synthesis contribute to the myocardial fibrotic response remains unknown. During the maturation phase of infarct healing, coating of infarct neovessels with pericytes plays an important role in scar stabilization. Implementation of therapeutic approaches targeting pericytes in the infarcted and remodeling heart remains challenging, due to the lack of systematic characterization of myocardial pericytes, their phenotypic heterogeneity and the limited knowledge on their functional role.</p>","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"H23-H31"},"PeriodicalIF":0.0,"publicationDate":"2019-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c6/34/VB-19-0007.PMC7439839.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38377217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Ex vivo</i> engineering of blood and lymphatic microvascular networks.","authors":"Jaana Schneider,&nbsp;Marianne Pultar,&nbsp;Wolfgang Holnthoner","doi":"10.1530/VB-19-0012","DOIUrl":"https://doi.org/10.1530/VB-19-0012","url":null,"abstract":"<p><p>Upon implantation, engineered tissues rely on the supply with oxygen and nutrients as well as the drainage of interstitial fluid. This prerequisite still represents one of the current challenges in the engineering and regeneration of tissues. Recently, different vascularization strategies have been developed. Besides technical approaches like 3D printing or laser processing and de-/recelluarization of natural scaffolds, mainly co-cultures of endothelial cells (ECs) with supporting cell types are being used. This mini-review provides a brief overview of different co-culture systems for the engineering of blood and lymphatic microvascular networks.</p>","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"H17-H22"},"PeriodicalIF":0.0,"publicationDate":"2019-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/17/ae/VB-19-0012.PMC7439851.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38377216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic vascular growth in the heart.","authors":"Ebba Brakenhielm,&nbsp;Vincent Richard","doi":"10.1530/VB-19-0006","DOIUrl":"https://doi.org/10.1530/VB-19-0006","url":null,"abstract":"<p><p>Despite tremendous efforts in preclinical research over the last decades, the clinical translation of therapeutic angiogenesis to grow stable and functional blood vessels in patients with ischemic diseases continues to prove challenging. In this mini review, we briefly present the current main approaches applied to improve pro-angiogenic therapies. Specific examples from research on therapeutic cardiac angiogenesis and arteriogenesis will be discussed, and finally some suggestions for future therapeutic developments will be presented.</p>","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"H9-H15"},"PeriodicalIF":0.0,"publicationDate":"2019-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38377215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic regulation of exercise-induced angiogenesis.","authors":"Tatiane Gorski,&nbsp;Katrien De Bock","doi":"10.1530/VB-19-0008","DOIUrl":"https://doi.org/10.1530/VB-19-0008","url":null,"abstract":"<p><p>Skeletal muscle relies on an ingenious network of blood vessels, which ensures optimal oxygen and nutrient supply. An increase in muscle vascularization is an early adaptive event to exercise training, but the cellular and molecular mechanisms underlying exercise-induced blood vessel formation are not completely clear. In this review, we provide a concise overview on how exercise-induced alterations in muscle metabolism can evoke metabolic changes in endothelial cells (ECs) that drive muscle angiogenesis. In skeletal muscle, angiogenesis can occur via sprouting and splitting angiogenesis and is dependent on vascular endothelial growth factor (VEGF) signaling. In the resting muscle, VEGF levels are controlled by the estrogen-related receptor γ (ERRγ). Upon exercise, the transcriptional coactivator peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC1α) orchestrates several adaptations to endurance exercise within muscle fibers and simultaneously promotes transcriptional activation of <i>Vegf</i> expression and increased muscle capillary density. While ECs are highly glycolytic and change their metabolism during sprouting angiogenesis in development and disease, a similar role for EC metabolism in exercise-induced angiogenesis in skeletal muscle remains to be elucidated. Nonetheless, recent studies have illustrated the importance of endothelial hydrogen sulfide and sirtuin 1 (SIRT1) activity for exercise-induced angiogenesis, suggesting that EC metabolic reprogramming may be fundamental in this process. We hypothesize that the exercise-induced angiogenic response can also be modulated by metabolic crosstalk between muscle and the endothelium. Defining the underlying molecular mechanisms responsible for skeletal muscle angiogenesis in response to exercise will yield valuable insight into metabolic regulation as well as the determinants of exercise performance.</p>","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"H1-H8"},"PeriodicalIF":0.0,"publicationDate":"2019-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/31/4c/VB-19-0008.PMC7439921.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38377214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improved endothelialization of small-diameter ePTFE vascular grafts through growth factor therapy.","authors":"Jarkko P Hytönen,&nbsp;Olli Leppänen,&nbsp;Jouni Taavitsainen,&nbsp;Petra Korpisalo,&nbsp;Svetlana Laidinen,&nbsp;Kari Alitalo,&nbsp;Jonas Wadström,&nbsp;Tuomas T Rissanen,&nbsp;Seppo Ylä-Herttuala","doi":"10.1530/VB-18-0001","DOIUrl":"https://doi.org/10.1530/VB-18-0001","url":null,"abstract":"<p><strong>Background: </strong>Prosthetic vascular grafts in humans characteristically lack confluent endothelialization regardless of the duration of implantation. Use of high-porosity grafts has been proposed as a way to induce endothelialization through transgraft capillarization, although early experiments failed to show increased healing in man.</p><p><strong>Objectives: </strong>We hypothesized that transduction of tissues around the prosthetic conduit with vectors encoding VEGF receptor-2 (VEGFR2) ligands would augment transinterstitial capillarization and induce luminal endothelialization of high-porosity ePTFE grafts.</p><p><strong>Methods: </strong>Fifty-two NZW rabbits received 87 ePTFE uni- or bilateral end-to-end interposition grafts in carotid arteries. Rabbits were randomized to local therapy with adenoviruses encoding AdVEGF-A165, AdVEGF-A109 or control AdLacZ and analyzed at 6 and 28 days after surgery by contrast-enhanced ultrasound and histology.</p><p><strong>Results: </strong>AdVEGF-A165 and AdVEGF-A109 dramatically increased perfusion in perigraft tissues at 6 days (14.2 ± 3.6 or 16.7 ± 2.6-fold increases, <i>P</i> < 0.05 and <i>P</i> < 0.01). At 28 days, the effect was no longer significantly higher than baseline. At 6 days, no luminal endothelialization was observed in any of the groups. At 28 days, AdVEGF-A109- and AdVEGF-A165-treated animals showed enhanced ingrowth of transinterstitial capillaries (66.0 ± 13.7% and 77.4 ± 15.7% of graft thickness vs 44.7 ± 24.4% in controls, <i>P</i> < 0.05) and improved luminal endothelialization (11.2 ± 26.3% and 11.4 ± 22.2%, AdVEGF-A109 and AdVEGF-A165 vs 0% in controls, <i>P</i> < 0.05). No increased stenosis was observed in the treatment groups as compared to LacZ controls.</p><p><strong>Conclusions: </strong>This study suggests that transient local overexpression of VEGFR2 ligands in the peri-implant tissues at the time of graft implantation is a novel strategy to increase endothelialization of high-porosity ePTFE vascular grafts and improve the patency of small-diameter vascular prostheses.</p>","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2019-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/82/ad/VB-18-0001.PMC7449264.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38374755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Why is a new journal dedicated to vascular biology required?","authors":"Paolo Madeddu","doi":"10.1530/VB-18-0005","DOIUrl":"https://doi.org/10.1530/VB-18-0005","url":null,"abstract":"The year 2018 marked the 110th anniversary of Goldmann’s discovery that vascularization is an active process in tissues1 and the 50th anniversary of the concomitant reports from Greenblatt and Shubik2 and Ehrmann and Knoth3 that soluble morphogenic factors are required for cancer angiogenesis. Many other radically transformative paradigms have been introduced in the last decades. To name a few, the molecular search for the identity of master regulators of vascular tone led to the discovery of the Endothelium-Derived Relaxing Factor (EDRF; i.e., NO4), while clinically inspired investigations led to the recognition of the pathophysiological relevance of neoangiogenesis in cancer and tissue healing. This brought about the proposal of blocking angiogenesis to halt tumor growth and stimulating angiogenesis to treat myocardial ischemia and heart failure5-7.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":"E1-E2"},"PeriodicalIF":0.0,"publicationDate":"2019-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7449262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38374758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improved endothelialization of small-diameter ePTFE grafts through growth factor therapy.","authors":"J. Hytönen, O. Leppänen, J. Taavitsainen, P. Korpisalo, S. Laidinen, K. Alitalo, J. Wadström, T. Rissanen, S. Ylä-Herttuala","doi":"10.1530/ec-18-0001","DOIUrl":"https://doi.org/10.1530/ec-18-0001","url":null,"abstract":"Background: Prosthetic vascular grafts in humans characteristically lack confluent endothelialization regardless the duration of implantation. Use of high-porosity grafts has been proposed as a way to induce endothelialization through transgraft capillarization, although early experiments failed to show increased healing in man. \u0000\u0000Objectives: We hypothesized that transduction of tissues around the prosthetic conduit with vectors encoding VEGF Receptor-2 (VEGFR2) ligands would augment transinterstitial capillarization and induce luminal endothelialization of high-porosity PTFE grafts.\u0000\u0000Methods: Fifty-two NZW rabbits received 87 ePTFE uni- or bilateral end-to-end interposition grafts in carotid arteries. Rabbits were randomized to local therapy with adenoviruses encoding AdVEGF-A165, AdVEGF-A109 or control AdLacZ and analyzed at 6 and 28d after surgery by contrast-enhanced ultrasound and histology. \u0000\u0000Results: AdVEGF-A165 and AdVEGF-A109 dramatically increased perfusion in perigraft tissues at 6d (14.2±3.6 or 16.7±2.6- fold increases, P<0.05 and P<0.01). At 28d the effect was no longer significantly higher than baseline. At 6d no luminal endothelialization was observed in any of the groups. At 28d, AdVEGF-A109 and AdVEGF-A165 treated animals showed enhanced ingrowth of transinterstitial capillaries (66.0±13.7% and 77.4±15.7% of graft thickness vs. 44.7±24.4% in controls, P<0.05) and improved luminal endothelialization (11.2±26.3% and 11.4±22.2%, AdVEGF-A109 and AdVEGF-A165 vs. 0% in controls, P<0.05). No increased stenosis was observed in the treatment groups as compared to LacZ controls. \u0000\u0000Conclusions: This study suggests that transient local overexpression of VEGFR2 ligands in the peri-implant tissues at time of graft implantation is a novel strategy to increase endothelialization of high-porosity ePTFE vascular grafts and improve the patency of small-diameter vascular prostheses.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44666263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}