Cited by 425Angiogenesis and VEGF in CancerFibroblast Growth Factor ResearchPregnancy and preeclampsia studies

The discovery of placenta growth factor and its biological activity

Open access
De Falco, Sandro·2012·Experimental and Molecular Medicine

Abstract

Angiogenesis is a complex biological phenomenon crucial for a correct embryonic development and for post-natal growth. In adult life, it is a tightly regulated process confined to the uterus and ovary during the different phases of the menstrual cycle and to the heart and skeletal muscles after prolonged and sustained physical exercise. Conversly, angiogenesis is one of the major pathological changes associated with several complex diseases like cancer, atherosclerosis, arthritis, diabetic retinopathy and age-related macular degeneration. Among the several molecular players involved in angiogenesis, some members of VEGF family, VEGF-A, VEGF-B and placenta growth factor (PlGF), and the related receptors VEGF receptor 1 (VEGFR-1, also known as Flt-1) and VEGF receptor 2 (VEGFR-2, also known as Flk-1 in mice and KDR in human) have a decisive role. In this review, we describe the discovery and molecular characteristics of PlGF, and discuss the biological role of this growth factor in physiological and pathological conditions.

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Registry

Crossref · 10.3858/emm.2012.44.1.025

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  • A similar pattern is observed for VEGF, stimulating angiogenesis and promoting capillary permeability, leading to expansion of the interstitium.

    “A similar pattern is observed for VEGF, stimulating angiogenesis and promoting capillary permeability,29 leading to expansion of the interstitium.30, 31”

    From Hypoalbuminemia: Pathogenesis and Clinical Significance (2019) · cites this paper as [29]

    The 'Role of PlGF in angiogenesis' section describes an angiogenic response elicited by VEGF-A, supporting that part of the claim. Its discussion of increased vascular leakiness concerns PlGF-overexpressing mice, not VEGF-induced capillary permeability. Expansion of the interstitium is attached to citations 30 and 31, rather than this source. (LLM, conf=0.82)

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  • VEGF expression and increased vascular permeability occur in infection, trauma, during fetal and postnatal growth, preparing for lactation, cancer, protein-losing enteropathy, and nephrotic syndrome.

    “VEGF expression and increased vascular permeability occur in infection,14, 35 trauma,15, 16, 36 during fetal and postnatal growth,29, 37, 38, 39 preparing for lactation,39, 40 cancer,41, 42 protein‐losing enteropathy,43 and nephrotic syndrome44, 45 (Table 1).”

    From Hypoalbuminemia: Pathogenesis and Clinical Significance (2019) · cites this paper as [29]

    The Abstract (page unavailable) links VEGF-family factors to angiogenesis during embryonic and postnatal growth and in cancer. The Role of PlGF in angiogenesis section reports increased vascular leakiness in mice overexpressing PlGF, but does not establish the claimed combination of VEGF expression and increased permeability across those settings. The copy does not address preparation for lactation, protein-losing enteropathy, or nephrotic syndrome. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • In pregnancy, serum albumin concentration decreases, vascular permeability increases, absolute synthesis increases, distribution volume increases, and VEGF increases.

    “Pregnancy 1st, 2nd, 3rd trimester | ↓ to ↓↓ | ↑ to↑↑ | ↑ | NA | NA | ↑ to↑↑ | ↑29 | Increasing permeability and distribution volume in the course of pregnancy”

    From Hypoalbuminemia: Pathogenesis and Clinical Significance (2019) · cites this paper as [29]

    The PlGF expression section (page unavailable) says placental growth factor is highly expressed throughout gestation and locates VEGF-A in placental tissue, but it does not report that VEGF increases during pregnancy. Searches for serum albumin, synthesis, distribution volume, and pregnancy-related vascular permeability found no passage addressing the claimed changes. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 1

  1. Semenza GL. Regulation of mammalian O2 homeostasis by hypoxia-inducible factor 1. Annu Rev Cell Dev Biol 1999; 15:551-78

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Authors
De Falco, S.
Affiliations
Angiogenesis Laboratory and Stem Cell Fate Laboratory, Institute of Genetics and Biophysics, 'Adriano Buzzati-Traverso' - CNR - Via Pietro Castellino, 111, 80131 Napoli, Italy.
Venue
Experimental and Molecular Medicine
Published
2012
Volume
44
Issue
1
Pages
1
ISSN
  • 1226-3613 (ISSN-L)
  • 2092-6413
OpenAlex
W2097881605
Cited by
425
References
99
Citations by year
2026: 10 · 2025: 33 · 2024: 34 · 2023: 39 · 2022: 35 · 2021: 28 · 2020: 38 · 2019: 44 · 2018: 35 · 2017: 32 · 2016: 22 · 2015: 23 · 2014: 35 · 2013: 14 · 2012: 2
FWCI
2.16
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Experimental & Molecular Medicine (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Associazione Italiana per la Ricerca sul Cancro
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Keywords
placental growth factor, angiogenesis, VEGF family, VEGF receptor 1, VEGF receptor 2, Flt-1, Flk-1, KDR, VEGF-A, VEGF-B, biological activity, pathogenesis
MeSH terms
Placenta Growth Factor, Animals, Female, Humans, Neovascularization, Pathologic, Nitric Oxide, Placenta, Pregnancy, Pregnancy Proteins, Mice, Knockout, Gene Expression Regulation, Developmental, Neovascularization, Physiologic, Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factor A, Endothelial Cells, Mice

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