Therapeutic lymphangiogenesis after myocardial infarction: vascular endothelial growth factor-C paves the way

Goichberg, Polina

doi:10.21037/jtd.2016.07.34

Cited by 5 publications

(5 citation statements)

References 19 publications

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“…Recently, lymphangiogenesis has been implicated in various pathophysiological processes, including micro-edema, fibrosis after MI, and heart failure. Indeed, the new cardiac lymphatic vessels formed after MI remove excess fluid, cytokines, and cell debris and regulate the immune reaction in the injured area, resulting in the stabilization of scar tissue and improvements in cardiac function ( Goichberg, 2016 ; Henri et al., 2016 ). Sema3E-PlexinD1 signaling may modulate these lymphangiogenic responses by antagonizing other semaphorin ligands and/or regional lymphangiogenic factors, including VEGF-C ( Klotz et al., 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery

et al. 2021

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Summary Blood and lymphatic vessels surrounding the heart develop through orchestrated processes from cells of different origins. In particular, cells around the outflow tract which constitute a primordial transient vasculature, referred to as aortic subepicardial vessels, are crucial for the establishment of coronary artery stems and cardiac lymphatic vessels. Here, we revealed that the epicardium and pericardium-derived Semaphorin 3E (Sema3E) and its receptor, PlexinD1, play a role in the development of the coronary stem, as well as cardiac lymphatic vessels. In vitro analyses demonstrated that Sema3E may demarcate areas to repel PlexinD1-expressing lymphatic endothelial cells, resulting in proper coronary and lymphatic vessel formation. Furthermore, inactivation of Sema3E-PlexinD1 signaling improved the recovery of cardiac function by increasing reactive lymphangiogenesis in an adult mouse model of myocardial infarction. These findings may lead to therapeutic strategies that target Sema3E-PlexinD1 signaling in coronary artery diseases.

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Section: Discussionmentioning

confidence: 99%

Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery

et al. 2021

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“…Moreover, immunologic and superantigenic stimuli can induce the release of proangiogenic (VEGF-A) and lymphangiogenic (VEGF-C) factors from primary human cardiac mast cells [66,226]. Notably, the production of VEGF-C by human cardiac mast cells can exert a potentially cardioprotective effect, since activation of the cardiac lymphatics improves the resolution of inflammation [67,236] and has an essential role in counteracting myocardial edema [68,237,238]. Interestingly, the activation of the protease activated receptor 2 (PAR-2) on cardiomyocytes by tryptase following experimental myocardial infarction also can exert a net protective effect [219].…”

Section: Mast Cells In Cardiovascular Diseasesmentioning

confidence: 99%

Future Needs in Mast Cell Biology

Varricchi

Paulis

Marone

et al. 2019

IJMS

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The pathophysiological roles of mast cells are still not fully understood, over 140 years since their description by Paul Ehrlich in 1878. Initial studies have attempted to identify distinct “subpopulations” of mast cells based on a relatively small number of biochemical characteristics. More recently, “subtypes” of mast cells have been described based on the analysis of transcriptomes of anatomically distinct mouse mast cell populations. Although mast cells can potently alter homeostasis, in certain circumstances, these cells can also contribute to the restoration of homeostasis. Both solid and hematologic tumors are associated with the accumulation of peritumoral and/or intratumoral mast cells, suggesting that these cells can help to promote and/or limit tumorigenesis. We suggest that at least two major subsets of mast cells, MC1 (meaning anti-tumorigenic) and MC2 (meaning pro-tumorigenic), and/or different mast cell mediators derived from otherwise similar cells, could play distinct or even opposite roles in tumorigenesis. Mast cells are also strategically located in the human myocardium, in atherosclerotic plaques, in close proximity to nerves and in the aortic valve. Recent studies have revealed evidence that cardiac mast cells can participate both in physiological and pathological processes in the heart. It seems likely that different subsets of mast cells, like those of cardiac macrophages, can exert distinct, even opposite, effects in different pathophysiological processes in the heart. In this chapter, we have commented on possible future needs of the ongoing efforts to identify the diverse functions of mast cells in health and disease.

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“…The first studies investigating the cardiac effects of therapeutic lymphangiogenesis were performed in experimental MI models in rodents 131 : Klotz et al used repeated intraperitoneal injections in mice of naked recombinant human VEGFR3-selective VEGF-CC156S mutant 12 , whereas Henri et al used intramyocardial spatiotemporally-controlled biopolymeric delivery in rats of recombinant rat VEGFR3-selective VEGF-CC152S mutant 13 . Modulation of cardiac lymphangiogenesis post-MI by apelin 96 or by cell therapy with bone marrow-derived endothelial progenitor cells (EPC) 94 have also been reported.…”

Section: Therapeutic Stimulation Of Cardiac Lymphangiogenesismentioning

confidence: 99%

Cardiac lymphatics in health and disease

2018

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The lymphatic vasculature, which accompanies the blood vasculature in most organs, is indispensable in for maintenance of tissue fluid homeostasis, immune cell trafficking and nutritional lipid uptake and transport, as well as reverse cholesterol transport. In this review, we discuss the physiological role of lymphatics in the heart, in maintenance of cardiac health, and describe alterations of lymphatic structure and function that occur in cardiovascular pathology, including atherosclerosis and myocardial infarction. We further discuss briefly the role that immune cells may play in the regulation of lymphatic growth (lymphangiogenesis) and function. Finally, we provide recent examples of how the cardiac lymphatics may be targeted therapeutically to restore lymphatic drainage in the heart in order to limit myocardial edema and chronic inflammation. Key points  Cardiac lymphatics display a dynamic range of fluid uptake and transport, linked to cardiac contractility and heart rate  Cardiac lymphatics undergo significant remodeling in several cardiovascular diseases, which can alter the lymphatic drainage capacity in the heart  Insufficient lymphangiogenesis may contribute to the buildup of atherosclerotic lesions in large arteries due to accumulation of both lipids and activated immune cells  Immune cells contribute to the process of lymphatic remodeling by stimulating or inhibiting lymphangiogenesis  Therapeutic stimulation of cardiac lymphangiogenesis after myocardial infarction leads to accelerated resolution of myocardial edema and inflammation, promoting cardiac recovery

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Therapeutic lymphangiogenesis after myocardial infarction: vascular endothelial growth factor-C paves the way

Cited by 5 publications

References 19 publications

Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery

Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery

Future Needs in Mast Cell Biology

Cardiac lymphatics in health and disease

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