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Biological basis of angiogenesis and role of vascular endothelial growth factor-D
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
Tumor growth and metastatic spread are processes that depend strictly on the activity of VEGFs. A tumor mass that does not express VEGF does not grow more than a few millimeters in diameter. Convincing experiments have demonstrated that specific antibodies against VEGF suppress tumor growth in vivo24. More recently, it has been shown that both VEGF-C and VEGF-D induce lymphatic metastatic spread25–27. Inhibition of angiogenesis and/or lymphangiogenesis represents one of the most promising therapeutic strategies to inhibit cancer growth and metastatic spread.
Milroy Disease
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Being a chronic and progressive disease, lymphedema may be primary or secondary. Accounting for about 10% of lymphedema cases, primary lymphedema represents a failure in the development of the lymphatic system (lymphangiogenesis), leading to structural or functional abnormalities in the lymphatic system and impaired maintenance of interstitial fluid balance. Being an important cause of primary lymphedema, Milroy disease (i.e., congenital lymphedema) is attributed to heterozygous mutations in the FLT4 (5q35.3) gene. Other potential causes of primary lymphedema include syndromic disorders (e.g., Turner or Noonan syndrome), systemic/visceral lymphatic abnormalities (localized or generalized lymphedema), disturbed growth and/or cutaneous/vascular anomalies (e.g., Proteus syndrome), and late-onset primary lymphedema [1].
How much pharmacological therapy can be incorporated in primary lymphedema management?
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
However, there is concern about the potential cancer-promoting effects of drugs, which stimulate lymphangiogenesis, when they are used to treat lymphedema secondary to cancer treatment.14 However, a role in the treatment of primary lymphedema may be possible. As yet, no clinical trials have been reported.
M2b macrophages stimulate lymphangiogenesis to reduce myocardial fibrosis after myocardial ischaemia/reperfusion injury
Published in Pharmaceutical Biology, 2022
Cuiping Wang, Yuan Yue, Suiqing Huang, Keke Wang, Xiao Yang, Jiantao Chen, Jiaxing Huang, Zhongkai Wu
Macrophages produce VEGFC to promote lymphangiogenesis (Watari et al. 2008; Yamashita et al. 2009). The phenotypic heterogeneity of macrophages relates to unique functions specific to the local microenvironment. In a mouse model of renal fibrosis, a VEGFR3 inhibitor down-regulated the expression of VEGFC by M1 macrophages to reduce lymphangiogenesis and ameliorate tubule-interstitial fibrosis. M1 macrophages can cause chronic inflammation-induced lymphangiogenesis, which worsens renal fibrosis (Hwang et al. 2019). Our previous study showed that M2b macrophages can significantly reduce the level of cardiac troponin I (cTnI) and the infarct area during the early period of MI/RI (Yue et al. 2017). Whether M2b macrophages can inhibit long-term cardiac fibrosis after MI/RI has not been studied.
Sentinel Lymph Node Biopsy after Previous Radical Lymphadenectomy of the Same Lymph Node Basin
Published in Journal of Investigative Surgery, 2022
Alberto Julius Alves Wainstein, Lucas Dias Cândido, Ana Paula Drummond-Lage
Previous studies of SLNB excluded the patients who had undergone prior surgery in a LN basin based on the assumption that prior surgery might complicate the identification of the SN or disrupt lymphatic channels from the recurrent site [27–29]. However, primary tumors can induce lymphangiogenesis and new paths of lymphatic vessels are developed. Based on this concept, two major hypotheses were proposed. In the first case, after radical LN dissection, small lymphatic vessels enlarged to facilitate lymphatic drainage of the operated member. Since there are no LNs, lymphatic drainage is driven to the next chain, that is, from the inguinal/femoral chain to the iliac chain, from axillary levels I and II to III [23]. In the second one, secondary tumors or recurrences produce growth factors, previously known as angiogenesis factors, such as PDGF-β and VEGF-A [30,31].
Updates on the Management of Ocular Vasculopathies with VEGF Inhibitor Conbercept
Published in Current Eye Research, 2020
Huan Liu, Yue Ma, Hong-Chang Xu, Li-Ying Huang, Li-Ying Zhai, Xiao-Rong Zhang
The binding of VEGF-A to VEGFR-2 promotes angiogenesis by stimulating vascular endothelial cell migration, proliferation, and survival, as well as vessel dilation and permeability.,1,24 The binding of VEGF-C (or – D) to VEGFR-2 or −3 promotes lymphangiogenesis in a similar fashion.25 VEGF binds to receptors expressed on endothelial cells: VEGF receptor 1 (FLT1) and VEGF receptor 2 (KDR). FLT1 and KDR are highly related transmembrane tyrosine kinases that use their ectodomains to bind VEGF, which activates the intrinsic tyrosine kinase activity of their cytodomains and initiates intracellular signaling. The receptor-binding determinants of VEGF are localized in the N-terminal portion (amino acids 1–110), and FLT1 and KDR bind to different sites on VEGF.26,27