KS-WNK1 is required for the renal response to extreme changes in potassium intake-Reference-Cited by-同舟云学术

KS-WNK1 is required for the renal response to extreme changes in potassium intake

Published:2024-03-01 Issue:3 Volume:326 Page:F460-F476
ISSN:1931-857X
Container-title:American Journal of Physiology-Renal Physiology
language:en
Short-container-title:American Journal of Physiology-Renal Physiology

Author:

Bahena-Lopez Jessica Paola¹²,Vergara Laura³^ORCID,de la-Peña Valeria¹³^ORCID,Gutierrez-Gallardo Miguel A.¹²^ORCID,López-Ibargüen Paulina¹,García Janeth Alejandra⁴^ORCID,Contreras-Carbajal Héctor¹,Vázquez Norma⁴^ORCID,Rincón-Heredia Ruth⁵^ORCID,Masso Felipe³^ORCID,Bobadilla Norma A.¹⁴^ORCID,Castañeda-Bueno María¹^ORCID,Ellison David H.⁶⁷^ORCID,Gamba Gerardo¹²⁴^ORCID,Chávez-Canales María³^ORCID

Affiliation:

1. Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico

2. MD/PhD program (Programa de Estudios Combinados en Medicina), Faculty of Medicine, Universidad Nacional Autónoma de México, Mexico City, Mexico

3. Unidad de Investigación UNAM-INCICH, Instituto Nacional de Cardiología Ignacio Chávez and Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City, Mexico

4. Molecular Physiology Unit, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City, Mexico

5. Unidad de Imagenología, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico

6. Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon, United States

7. Oregon Clinical and Translational Research Institute, Oregon Health and Science University, Portland, Oregon, United States

Abstract

The findings of this study demonstrate that kidney-specific with-no-lysine kinase 1 plays a role in regulating urinary electrolyte excretion during extreme changes in potassium intake, such as those occurring in wildlife.

Funder

Consejo Nacional de Ciencia y Tecnología

Foundation for the National Institutes of Health

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

UNAM | Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México

Publisher

American Physiological Society

Link

https://journals.physiology.org/doi/pdf/10.1152/ajprenal.00235.2023

Reference27 articles.

1. Multiple Promoters in the WNK1 Gene: One Controls Expression of a Kidney-Specific Kinase-Defective Isoform

2. Pathogenesis of pseudohypoaldosteronism type 2 by WNK1 mutations

3. Dominant-negative regulation of WNK1 by its kidney-specific kinase-defective isoform

4. Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension

5. Downregulation of NCC and NKCC2 cotransporters by kidney-specific WNK1 revealed by gene disruption and transgenic mouse models

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