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肽Lv与血管生成:一种新发现的血管生成肽。

Peptide Lv and Angiogenesis: A Newly Discovered Angiogenic Peptide.

作者信息

Pham Dylan L, Cox Kelsey, Ko Michael L, Ko Gladys Y-P

机构信息

Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843, USA.

Department of Medical Physiology, School of Medicine, Texas A&M University, Bryan, TX 77807, USA.

出版信息

Biomedicines. 2024 Dec 15;12(12):2851. doi: 10.3390/biomedicines12122851.

DOI:10.3390/biomedicines12122851
PMID:39767758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11672992/
Abstract

Peptide Lv is a small endogenous secretory peptide with ~40 amino acids and is highly conserved among certain several species. While it was first discovered that it augments L-type voltage-gated calcium channels (LTCCs) in neurons, thus it was named peptide "Lv", it can bind to vascular endothelial growth factor receptor 2 (VEGFR2) and has VEGF-like activities, including eliciting vasodilation and promoting angiogenesis. Not only does peptide Lv augment LTCCs in neurons and cardiomyocytes, but it also promotes the expression of intermediate-conductance K channels (K3.1) in vascular endothelial cells. Peptide Lv is upregulated in the retinas of patients with early proliferative diabetic retinopathy, a disease involving pathological angiogenesis. This review will provide an overview of peptide Lv, its known bioactivities in vitro and in vivo, and its clinical relevance, with a focus on its role in angiogenesis. As there is more about peptide Lv to be explored, this article serves as a foundation for possible future developments of peptide Lv-related therapeutics to treat or prevent diseases.

摘要

肽Lv是一种约含40个氨基酸的内源性小分泌肽,在某些物种中高度保守。最初发现它可增强神经元中的L型电压门控钙通道(LTCCs),因此被命名为肽“Lv”,它能与血管内皮生长因子受体2(VEGFR2)结合并具有类VEGF活性,包括引起血管舒张和促进血管生成。肽Lv不仅能增强神经元和心肌细胞中的LTCCs,还能促进血管内皮细胞中中等电导钾通道(K3.1)的表达。在早期增殖性糖尿病视网膜病变(一种涉及病理性血管生成的疾病)患者的视网膜中,肽Lv表达上调。本综述将概述肽Lv、其在体外和体内已知的生物活性及其临床相关性,重点关注其在血管生成中的作用。由于关于肽Lv还有更多有待探索之处,本文为未来开发与肽Lv相关的治疗方法以治疗或预防疾病奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/c707f983fc50/biomedicines-12-02851-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/ec9cdeaad25c/biomedicines-12-02851-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/963c30a5d9b6/biomedicines-12-02851-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/b52e3d57f11c/biomedicines-12-02851-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/c707f983fc50/biomedicines-12-02851-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/ec9cdeaad25c/biomedicines-12-02851-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/963c30a5d9b6/biomedicines-12-02851-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/b52e3d57f11c/biomedicines-12-02851-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0859/11672992/c707f983fc50/biomedicines-12-02851-g004.jpg

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Peptide Lv and Angiogenesis: A Newly Discovered Angiogenic Peptide.肽Lv与血管生成:一种新发现的血管生成肽。
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Peptide Lv augments intermediate-conductance calcium-dependent potassium channels (KCa3.1) in endothelial cells to promote angiogenesis.肽 Lv 通过增强内皮细胞中的中电导钙依赖性钾通道(KCa3.1)促进血管生成。
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引用本文的文献

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本文引用的文献

1
Peptide Lv Promotes Trafficking and Membrane Insertion of K3.1 through the MEK1-ERK and PI3K-Akt Signaling Pathways.肽 Lv 通过 MEK1-ERK 和 PI3K-Akt 信号通路促进 K3.1 的运输和膜插入。
Cells. 2023 Jun 17;12(12):1651. doi: 10.3390/cells12121651.
2
Peptide Lv augments intermediate-conductance calcium-dependent potassium channels (KCa3.1) in endothelial cells to promote angiogenesis.肽 Lv 通过增强内皮细胞中的中电导钙依赖性钾通道(KCa3.1)促进血管生成。
PLoS One. 2022 Oct 25;17(10):e0276744. doi: 10.1371/journal.pone.0276744. eCollection 2022.
3
Regulation of Tumor Necrosis Factor-α by Peptide Lv in Bone Marrow Macrophages and Synovium.
肽Lv对骨髓巨噬细胞和滑膜中肿瘤坏死因子-α的调控
Front Med (Lausanne). 2021 Jul 27;8:702126. doi: 10.3389/fmed.2021.702126. eCollection 2021.
4
Retinopathy of prematurity shows alterations in Vegfa isoform expression.早产儿视网膜病变表现出 Vegfa 同工型表达的改变。
Pediatr Res. 2022 Jun;91(7):1677-1685. doi: 10.1038/s41390-021-01646-9. Epub 2021 Jul 20.
5
Age-related macular degeneration.年龄相关性黄斑变性。
Nat Rev Dis Primers. 2021 May 6;7(1):31. doi: 10.1038/s41572-021-00265-2.
6
Endothelial ATP-Sensitive Potassium Channel Protects Against the Development of Hypertension and Atherosclerosis.内皮细胞三磷酸腺苷敏感性钾通道可预防高血压和动脉粥样硬化的发生。
Hypertension. 2020 Sep;76(3):776-784. doi: 10.1161/HYPERTENSIONAHA.120.15355. Epub 2020 Jul 13.
7
Endothelial TRPV4 channels and vasodilator reactivity.内皮细胞瞬时受体电位香草酸亚型4通道与血管舒张反应性。
Curr Top Membr. 2020;85:89-117. doi: 10.1016/bs.ctm.2020.01.007. Epub 2020 Feb 12.
8
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J Am Heart Assoc. 2019 Nov 19;8(22):e013673. doi: 10.1161/JAHA.119.013673. Epub 2019 Nov 8.
9
Trends and Challenges in Tumor Anti-Angiogenic Therapies.肿瘤抗血管生成治疗的趋势和挑战。
Cells. 2019 Sep 18;8(9):1102. doi: 10.3390/cells8091102.
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Angiogenesis: Managing the Culprits behind Tumorigenesis and Metastasis.血管生成:肿瘤发生和转移背后的元凶管理。
Medicina (Kaunas). 2018 Mar 25;54(1):8. doi: 10.3390/medicina54010008.