Defective coronary vessel organization and reduction of VEGF‐A in mouse embryonic hearts with gestational mild hypoxia

Cai, Lawrence X.; Alkassis, Fariz F.; Kasahara, Hideko

doi:10.1002/dvdy.149

Cited by 3 publications

(1 citation statement)

References 55 publications

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“…Annexin A1 (AnxA1) directly led cardiac macrophages to polarize to angiogenic and repair phenotypes, and stimulated cardiac macrophages to release large amounts of VEGF-A, thus inducing angiogenesis and cardiac repair (20). By contrast, one study revealed that mild hypoxia (14% O 2 ) did not induce coronary angiogenesis or VEGF-A expression in hearts of developing mice (21).…”

Section: Mechanisms Regulating the Level Of Vegf-a Upregulation Mechanism Of Vegf-amentioning

confidence: 99%

The Role of the VEGF Family in Coronary Heart Disease

Zhou

Zhu

Cui

et al. 2021

Front. Cardiovasc. Med.

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The vascular endothelial growth factor (VEGF) family, the regulator of blood and lymphatic vessels, is mostly investigated in the tumor and ophthalmic field. However, the functions it enjoys can also interfere with the development of atherosclerosis (AS) and further diseases like coronary heart disease (CHD). The source, regulating mechanisms including upregulation and downregulation, target cells/tissues, and known functions about VEGF-A, VEGF-B, VEGF-C, and VEGF-D are covered in the review. VEGF-A can regulate angiogenesis, vascular permeability, and inflammation by binding with VEGFR-1 and VEGFR-2. VEGF-B can regulate angiogenesis, redox, and apoptosis by binding with VEGFR-1. VEGF-C can regulate inflammation, lymphangiogenesis, angiogenesis, apoptosis, and fibrogenesis by binding with VEGFR-2 and VEGFR-3. VEGF-D can regulate lymphangiogenesis, angiogenesis, fibrogenesis, and apoptosis by binding with VEGFR-2 and VEGFR-3. These functions present great potential of applying the VEGF family for treating CHD. For instance, angiogenesis can compensate for hypoxia and ischemia by growing novel blood vessels. Lymphangiogenesis can degrade inflammation by providing exits for accumulated inflammatory cytokines. Anti-apoptosis can protect myocardium from impairment after myocardial infarction (MI). Fibrogenesis can promote myocardial fibrosis after MI to benefit cardiac recovery. In addition, all these factors have been confirmed to keep a link with lipid metabolism, the research about which is still in the early stage and exact mechanisms are relatively obscure. Because few reviews have been published about the summarized role of the VEGF family for treating CHD, the aim of this review article is to present an overview of the available evidence supporting it and give hints for further research.

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Section: Mechanisms Regulating the Level Of Vegf-a Upregulation Mechanism Of Vegf-amentioning

confidence: 99%

The Role of the VEGF Family in Coronary Heart Disease

Zhou

Zhu

Cui

et al. 2021

Front. Cardiovasc. Med.

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Hypoxia causes trophoblast cell ferroptosis to induce miscarriage through lnc-HZ06/HIF1α-SUMO/NCOA4 axis

Tian,

Xu,

Guo

et al. 2024

Redox Biology

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Gestational intermittent hyperoxia rescues murine genetic congenital heart disease in part

Doll

Pereira

Hashimi

et al. 2021

Sci Rep

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Cardiac development is a dynamic process, temporally and spatially. When disturbed, it leads to congenital cardiac anomalies that affect approximately 1% of live births. Genetic variants in several loci lead to anomalies, with the transcription factor NKX2-5 being one of the largest. However, there are also non-genetic factors that influence cardiac malformations. We examined the hypothesis that hyperoxia may be beneficial and can rescue genetic cardiac anomalies induced by an Nkx2-5 mutation. Intermittent mild hyperoxia (40% PO2) was applied for 10 h per day to normal wild-type female mice mated with heterozygous Nkx2-5 mutant males from gestational day 8.5 to birth. Hyperoxia therapy reduced excessive trabeculation in Nkx2-5 mutant mice compared to normoxic conditions (ratio of trabecular layer relative to compact layer area, normoxia 1.84 ± 0.07 vs. hyperoxia 1.51 ± 0.04) and frequency of muscular ventricular septal defects per heart (1.53 ± 0.32 vs. 0.68 ± 0.15); however, the incidence of membranous ventricular septal defects in Nkx2-5 mutant hearts was not changed. Nkx2-5 mutant embryonic hearts showed defective coronary vessel organization, which was improved by intermittent mild hyperoxia. The results of our study showed that mild gestational hyperoxia therapy rescued genetic cardiac malformation induced by Nkx2-5 mutation in part.

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Defective coronary vessel organization and reduction of VEGF‐A in mouse embryonic hearts with gestational mild hypoxia

Cited by 3 publications

References 55 publications

The Role of the VEGF Family in Coronary Heart Disease

The Role of the VEGF Family in Coronary Heart Disease

Hypoxia causes trophoblast cell ferroptosis to induce miscarriage through lnc-HZ06/HIF1α-SUMO/NCOA4 axis

Gestational intermittent hyperoxia rescues murine genetic congenital heart disease in part

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