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1.
Am J Physiol Heart Circ Physiol ; 326(6): H1396-H1401, 2024 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-38578238

RESUMO

Given the growing interest in the role of zinc in the onset and progression of diseases, there is a crucial demand for reliable methods to modulate zinc homeostasis. Using a dietary approach, we provide validated strategies to alter whole-body zinc in mice, applicable across species. For confirmation of zinc status, animal growth rates as well as plasma and urine zinc levels were evaluated. The accessible and cost-effective methodology outlined will increase scientific rigor, ensuring reproducibility in studies exploring the impact of zinc deficiency and repletion on the onset and progression of diseases.NEW & NOTEWORTHY This methods paper details dietary approaches to alter zinc homeostasis in rodents and qualitative and quantitative methods to ensure the zinc status of experimental animals. The outlined accessible and cost-effective protocol will elevate scientific rigor, ensuring reproducibility in studies exploring the impact of zinc deficiency and repletion on the onset and progression of a multitude of health conditions and diseases.


Assuntos
Zinco , Zinco/deficiência , Zinco/metabolismo , Zinco/urina , Zinco/sangue , Animais , Reprodutibilidade dos Testes , Camundongos , Camundongos Endogâmicos C57BL , Homeostase , Masculino
2.
bioRxiv ; 2024 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-38463970

RESUMO

Given the growing interest in the role of zinc in the onset and progression of diseases, there is a crucial demand for reliable methods to modulate zinc homeostasis. Using a dietary approach, we provide validated strategies to alter whole-body zinc in mice, applicable across species. For confirmation of zinc status, animal growth rates as well as plasma and urine zinc levels were evaluated. The accessible and cost-effective methodology outlined will increase scientific rigor, ensuring reproducibility in studies exploring the impact of zinc deficiency and repletion on the onset and progression of diseases.

3.
Aging Cell ; 22(12): e14019, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37960979

RESUMO

Recently, latent transforming growth factor beta binding protein 4 (LTBP4) was implicated in the pathogenesis of renal damage through its modulation of mitochondrial dynamics. The seminal article written by Su et al. entitled "LTBP4 (Latent Transforming Growth Factor Beta Binding Protein 4) Protects Against Renal Fibrosis via Mitochondrial and Vascular Impacts" uncovers LTBP4's renoprotective role against acute kidney injury via modulating mitochondrial dynamics. Recently, LTBP4 has emerged as a driver in the mitochondrial-dependent modulation of age-related organ pathologies. This article aims to expand our understanding of LTBP4's diverse roles in these diseases in the context of these recent findings.


Assuntos
Injúria Renal Aguda , Humanos , Proteínas de Ligação a TGF-beta Latente/metabolismo , Rim/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Mitocôndrias/metabolismo
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