ArticleBiomedicines2024
Unraveling the Complex Molecular Interplay and Vascular Adaptive Changes in Hypertension-Induced Kidney Disease.
Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Understanding Anterior Cruciate Ligament Adaptation: Structural, Mechanical, and Healing Considerations.Sports medicine (Auckland, N.Z.) · 2026Review
- Spatiotemporal APLNR Expression Dynamics During Oligodendroglial Remodeling of the Corpus Callosum in the Cuprizone Model.International journal of molecular sciences · 2026Article
- Review
- Therapeutic monoclonal antibodies for diabetic kidney disease: a narrative review from basic mechanisms to clinical evidence.Frontiers in endocrinology · 2026Review
- The Apelinergic System in Kidney Disease: Novel Perspectives.International journal of molecular sciences · 2025Review
- Unveiling Vascular Dynamics: Introducing theBiomedicines · 2025Article
- Association of quantitative renal surface nodularity with the renal dysfunction progression in patients with arterial hypertension.BMC medical imaging · 2025Article
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Direct simulation of hypertensive stress on endothelial cells: a streamlined model of in-vitro-hypertension.Frontiers in physiology · 2025Article
- Exploring the Molecular Modalities in the Pathogenesis of Diabetic Kidney Disease with a Focus on the Potential Therapeutic Implications.Biomedicines · 2024Review
- A Morphological and Behavioral Study of Demyelination and Remyelination in the Cuprizone Model: Insights into APLNR and NG2+ Cell Dynamics.International journal of molecular sciences · 2024Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate the role of the apelin receptor (APLNR), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF) in hypertension-induced renal damage. We used two groups of spontaneously hypertensive rats aged 6 and 12 months, representing different stages of AH, and compared them to age-matched normotensive controls. The kidney tissue samples were prepared through a well-established protocol. All data analysis was conducted with a dedicated software program. APLNR was localized in tubular epithelial cells and the endothelial cells of the glomeruli, with higher expression in older SHRs. The localization of nNOS and VEGF was similar. The expression of APLNR and nNOS increased with AH progression, while VEGF levels decreased. CD was lower in young SHRs compared to controls and decreased significantly in older SHRs in comparison to age-matched controls. Our statistical analysis revealed significant differences in molecule expression between age groups and varying correlations between the expression of the three molecules and CD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.