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Advances and Challenges of Molecular Research on Disease in Animal Models in Biomedicine

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 1246

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Guest Editor
Department of Physiology, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA
Interests: intrarenal renin-angiotensin system in hypertension and diabetes; impact of prorenin and prorenin receptor interactions in cardiovascular and renal diseases; translational research

Special Issue Information

Dear Colleagues,

Significant advances in our knowledge of animal models have contributed to the innovation of biomedical sciences through a better understanding of pathological, biological, and molecular mechanisms. Through murine, primate, porcine, and aquatic models, several cardiovascular, renal, neurological, behavioral, and oncological disorders are being better understood while developing new therapeutic approaches. They facilitate the development and testing of drugs, vaccines, organ transplants, and surgical techniques applicable to human and veterinary medicine. The broad range of species used in research has implied challenges and brought exponential advances in medicine, especially with the introduction of transgenic animals, and the implementation of nanotechnology and artificial intelligence.

The goal of this Special Issue on “Advances and Challenges of Molecular Research on Disease in Animal Models in Biomedicine” is to better understand novel molecular and therapeutic approaches and signaling molecules for studying pathologies that affect humans by replicating pathophysiological processes.

I want to invite you to submit original research communication and or review manuscripts focused, but not limited to, innovative findings and challenges of animal models contributing to enhancing the comprehensive view of the molecular pathophysiological mechanisms underlying the pathogenesis and progression of cardiovascular, renal, metabolic, oncology, and behavioral diseases. Studies involving animal models from different species are encouraged.

Dr. Minolfa C. Prieto
Guest Editor

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Keywords

  • animal models
  • cardiovascular disease
  • renal disease
  • metabolic, neurological, behavioral, and oncological disorders
  • pathophysiology
  • cell and molecular research

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Published Papers (1 paper)

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Research

19 pages, 3524 KiB  
Article
OXGR1-Dependent (Pro)Renin Receptor Upregulation in Collecting Ducts of the Clipped Kidney Contributes to Na+ Balance in Goldblatt Hypertensive Mice
by Pilar Cárdenas, Camila Nuñez-Allimant, Katherin Silva, Catalina Cid-Salinas, Allison C. León, Zoe Vallotton, Ramón A. Lorca, Lilian Caroline Gonçalves de Oliveira, Dulce E Casarini, Carlos Céspedes, Minolfa C. Prieto and Alexis A. Gonzalez
Int. J. Mol. Sci. 2024, 25(18), 10045; https://doi.org/10.3390/ijms251810045 - 18 Sep 2024
Viewed by 900
Abstract
The two-kidney, one-clip (2K1C) Goldblatt rodent model elicits a reduction in renal blood flow (RBF) in the clipped kidney (CK). The reduced RBF and oxygen bio-ability causes the accumulation of the tricarboxylic cycle intermediary, α-ketoglutarate, which activates the oxoglutarate receptor-1 (OXGR1). In the [...] Read more.
The two-kidney, one-clip (2K1C) Goldblatt rodent model elicits a reduction in renal blood flow (RBF) in the clipped kidney (CK). The reduced RBF and oxygen bio-ability causes the accumulation of the tricarboxylic cycle intermediary, α-ketoglutarate, which activates the oxoglutarate receptor-1 (OXGR1). In the kidney, OXGR1 is abundantly expressed in intercalated cells (ICs) of the collecting duct (CD), thus contributing to sodium transport and electrolyte balance. The (pro)renin receptor (PRR), a member of the renin–angiotensin system (RAS), is a key regulator of sodium reabsorption and blood pressure (BP) that is expressed in ICs. The PRR is upregulated in 2K1C rats. Here, we tested the hypothesis that chronic reduction in RBF in the CK leads to OXGR1-dependent PRR upregulation in the CD and alters sodium balance and BP in 2K1C mice. To determine the role of OXGR1 in regulating the PRR in the CDs during renovascular hypertension, we performed 2K1C Goldblatt surgery (clip = 0.13 mm internal gap, 14 days) in two groups of male mice: (1) mice treated with Montelukast (OXGR1 antagonist; 5 mg/Kg/day); (2) OXGR1−/− knockout mice. Wild-type and sham-operated mice were used as controls. After 14 days, 2K1C mice showed increased systolic BP (SBP) (108 ± 11 vs. control 82 ± 5 mmHg, p < 0.01) and a lower natriuretic response after the saline challenge test. The CK group showed upregulation of erythropoietin, augmented α-ketoglutarate, and increased PRR expression in the renal medulla. The CK of OXGR1 knockout mice and mice subjected to the OXGR1 antagonist elicited impaired PRR upregulation, attenuated SBP, and better natriuretic responses. In 2K1C mice, the effect of reduced RBF on the OXGR1-dependent PRR upregulation in the CK may contribute to the anti-natriuretic and increased SBP responses. Full article
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