The discovery of placenta growth factor and its biological activity
Open accessAbstract
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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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)
Experimental — accuracy not yet measuredVEGF 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 measuredIn 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)
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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
- PMC
- PMC3277892
- 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
- gold
- doi.org
- 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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