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Article

The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats

1
Departamento de Fisiología, Facultad de Medicina, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Universidad Complutense de Madrid, 28040 Madrid, Spain
2
Institut de Recerca del Hospital de la Santa Creu i Sant Pau, 08025 Barcelona, Spain
3
Instituto de Investigación Biomédica Sant Pau (IB Sant Pau), 08025 Barcelona, Spain
4
Ciber de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III, 28220 Majadahonda, Spain
5
Instituto de Biología y Genética Molecular, CSIC-Universidad de Valladolid, 47002 Valladolid, Spain
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this study.
These authors contributed equally to this study.
Academic Editor: Judith Haendeler
Antioxidants 2021, 10(8), 1274; https://doi.org/10.3390/antiox10081274
Received: 1 July 2021 / Revised: 4 August 2021 / Accepted: 9 August 2021 / Published: 11 August 2021
(This article belongs to the Special Issue Oxidative Stress in Obesity)
We have evaluated the role of mitochondrial oxidative stress and its association with endoplasmic reticulum (ER) stress activation in the progression of obesity-related cardiovascular fibrosis. MitoQ (200 µM) was orally administered for 7 weeks to male Wistar rats that were fed a high-fat diet (HFD, 35% fat) or a control diet (CT, 3.5% fat). Obese animals presented cardiovascular fibrosis accompanied by increased levels of extracellular matrix proteins and profibrotic mediators. These alterations were associated with ER stress activation characterized by enhanced levels (in heart and aorta vs. CT group, respectively) of immunoglobulin binding protein (BiP; 2.1-and 2.6-fold, respectively), protein disulfide-isomerase A6 (PDIA6; 1.9-fold) and CCAAT-enhancer-binding homologous protein (CHOP; 1.5- and 1.8-fold, respectively). MitoQ treatment was able to prevent (p < 0.05) these modifications at cardiac and aortic levels. MitoQ (5 nM) and the ER stress inhibitor, 4-phenyl butyric acid (4 µM), were able to block the prooxidant and profibrotic effects of angiotensin II (Ang II, 10−6 M) in cardiac and vascular cells. Therefore, the data show a crosstalk between mitochondrial oxidative stress and ER stress activation, which mediates the development of cardiovascular fibrosis in the context of obesity and in which Ang II can play a relevant role. View Full-Text
Keywords: cardiovascular fibrosis; endoplasmic reticulum stress; mitochondrial oxidative stress; obesity cardiovascular fibrosis; endoplasmic reticulum stress; mitochondrial oxidative stress; obesity
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MDPI and ACS Style

Souza-Neto, F.V.; Jiménez-González, S.; Delgado-Valero, B.; Jurado-López, R.; Genty, M.; Romero-Miranda, A.; Rodríguez, C.; Nieto, M.L.; Martínez-Martínez, E.; Cachofeiro, V. The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats. Antioxidants 2021, 10, 1274. https://doi.org/10.3390/antiox10081274

AMA Style

Souza-Neto FV, Jiménez-González S, Delgado-Valero B, Jurado-López R, Genty M, Romero-Miranda A, Rodríguez C, Nieto ML, Martínez-Martínez E, Cachofeiro V. The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats. Antioxidants. 2021; 10(8):1274. https://doi.org/10.3390/antiox10081274

Chicago/Turabian Style

Souza-Neto, Francisco V., Sara Jiménez-González, Beatriz Delgado-Valero, Raquel Jurado-López, Marie Genty, Ana Romero-Miranda, Cristina Rodríguez, María L. Nieto, Ernesto Martínez-Martínez, and Victoria Cachofeiro. 2021. "The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats" Antioxidants 10, no. 8: 1274. https://doi.org/10.3390/antiox10081274

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