Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C

Cardiorenal syndrome (CRS) is a pathological link between the kidneys and heart, in which an insult in a kidney or heart leads the other organ to incur damage. CRS is classified into five subtypes, and type 3 (CRS3) is characterized by acute kidney injury as a precursor to subsequent cardiovascular...

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Autores principales:	Raquel Silva Neres-Santos, Carolina Victoria Cruz Junho, Karine Panico, Wellington Caio-Silva, Joana Claudio Pieretti, Juliana Almeida Tamashiro, Amedea Barozzi Seabra, César Augusto João Ribeiro, Marcela Sorelli Carneiro-Ramos
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	CRS3 mitochondria nitric oxide mitochondrial dynamics vitamin C Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/979e6cac8d9b4da988eaa9d8ab58d65e
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spelling	oai:doaj.org-article:979e6cac8d9b4da988eaa9d8ab58d65e2021-11-25T17:10:33ZMitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C10.3390/cells101130292073-4409https://doaj.org/article/979e6cac8d9b4da988eaa9d8ab58d65e2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3029https://doaj.org/toc/2073-4409Cardiorenal syndrome (CRS) is a pathological link between the kidneys and heart, in which an insult in a kidney or heart leads the other organ to incur damage. CRS is classified into five subtypes, and type 3 (CRS3) is characterized by acute kidney injury as a precursor to subsequent cardiovascular changes. Mitochondrial dysfunction and oxidative and nitrosative stress have been reported in the pathophysiology of CRS3. It is known that vitamin C, an antioxidant, has proven protective capacity for cardiac, renal, and vascular endothelial tissues. Therefore, the present study aimed to assess whether vitamin C provides protection to heart and the kidneys in an in vivo CRS3 model. The unilateral renal ischemia and reperfusion (IR) protocol was performed for 60 min in the left kidney of adult mice, with and without vitamin C treatment, immediately after IR or 15 days after IR. Kidneys and hearts were subsequently collected, and the following analyses were conducted: renal morphometric evaluation, serum urea and creatinine levels, high-resolution respirometry, amperometry technique for NO measurement, gene expression of mitochondrial dynamic markers, and NOS. The analyses showed that the left kidney weight was reduced, urea and creatinine levels were increased, mitochondrial oxygen consumption was reduced, NO levels were elevated, and Mfn2 expression was reduced after 15 days of IR compared to the sham group. Oxygen consumption and NO levels in the heart were also reduced. The treatment with vitamin C preserved the left kidney weight, restored renal function, reduced NO levels, decreased iNOS expression, elevated constitutive NOS isoforms, and improved oxygen consumption. In the heart, oxygen consumption and NO levels were improved after vitamin C treatment, whereas the three NOS isoforms were overexpressed. These data indicate that vitamin C provides protection to the kidneys and some beneficial effects to the heart after IR, indicating it may be a preventive approach against cardiorenal insults.Raquel Silva Neres-SantosCarolina Victoria Cruz JunhoKarine PanicoWellington Caio-SilvaJoana Claudio PierettiJuliana Almeida TamashiroAmedea Barozzi SeabraCésar Augusto João RibeiroMarcela Sorelli Carneiro-RamosMDPI AGarticleCRS3mitochondrianitric oxidemitochondrial dynamicsvitamin CBiology (General)QH301-705.5ENCells, Vol 10, Iss 3029, p 3029 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	CRS3 mitochondria nitric oxide mitochondrial dynamics vitamin C Biology (General) QH301-705.5
spellingShingle	CRS3 mitochondria nitric oxide mitochondrial dynamics vitamin C Biology (General) QH301-705.5 Raquel Silva Neres-Santos Carolina Victoria Cruz Junho Karine Panico Wellington Caio-Silva Joana Claudio Pieretti Juliana Almeida Tamashiro Amedea Barozzi Seabra César Augusto João Ribeiro Marcela Sorelli Carneiro-Ramos Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C
description	Cardiorenal syndrome (CRS) is a pathological link between the kidneys and heart, in which an insult in a kidney or heart leads the other organ to incur damage. CRS is classified into five subtypes, and type 3 (CRS3) is characterized by acute kidney injury as a precursor to subsequent cardiovascular changes. Mitochondrial dysfunction and oxidative and nitrosative stress have been reported in the pathophysiology of CRS3. It is known that vitamin C, an antioxidant, has proven protective capacity for cardiac, renal, and vascular endothelial tissues. Therefore, the present study aimed to assess whether vitamin C provides protection to heart and the kidneys in an in vivo CRS3 model. The unilateral renal ischemia and reperfusion (IR) protocol was performed for 60 min in the left kidney of adult mice, with and without vitamin C treatment, immediately after IR or 15 days after IR. Kidneys and hearts were subsequently collected, and the following analyses were conducted: renal morphometric evaluation, serum urea and creatinine levels, high-resolution respirometry, amperometry technique for NO measurement, gene expression of mitochondrial dynamic markers, and NOS. The analyses showed that the left kidney weight was reduced, urea and creatinine levels were increased, mitochondrial oxygen consumption was reduced, NO levels were elevated, and Mfn2 expression was reduced after 15 days of IR compared to the sham group. Oxygen consumption and NO levels in the heart were also reduced. The treatment with vitamin C preserved the left kidney weight, restored renal function, reduced NO levels, decreased iNOS expression, elevated constitutive NOS isoforms, and improved oxygen consumption. In the heart, oxygen consumption and NO levels were improved after vitamin C treatment, whereas the three NOS isoforms were overexpressed. These data indicate that vitamin C provides protection to the kidneys and some beneficial effects to the heart after IR, indicating it may be a preventive approach against cardiorenal insults.
format	article
author	Raquel Silva Neres-Santos Carolina Victoria Cruz Junho Karine Panico Wellington Caio-Silva Joana Claudio Pieretti Juliana Almeida Tamashiro Amedea Barozzi Seabra César Augusto João Ribeiro Marcela Sorelli Carneiro-Ramos
author_facet	Raquel Silva Neres-Santos Carolina Victoria Cruz Junho Karine Panico Wellington Caio-Silva Joana Claudio Pieretti Juliana Almeida Tamashiro Amedea Barozzi Seabra César Augusto João Ribeiro Marcela Sorelli Carneiro-Ramos
author_sort	Raquel Silva Neres-Santos
title	Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C
title_short	Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C
title_full	Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C
title_fullStr	Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C
title_full_unstemmed	Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C
title_sort	mitochondrial dysfunction in cardiorenal syndrome 3: renocardiac effect of vitamin c
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/979e6cac8d9b4da988eaa9d8ab58d65e
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Mitochondrial Dysfunction in Cardiorenal Syndrome 3: Renocardiac Effect of Vitamin C

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