Sulforaphane prevents angiotensin II-induced cardiomyopathy by activation of Nrf2 via stimulating the Akt/GSK-3ß/Fyn pathway
Xin Y, Bai Y, Jiang X, Zhou S, Wang Y, Wintergerst KA, Cui T, Ji H, Tan Y, Cai L
Redox biology · 147 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Animales
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Organización sin fines de lucro
- American Diabetes Association
- Gobierno
- National Natural Science Foundation of China
- Universidad u hospital
- Jilin University
- Gobierno
- National Center for Complementary and Integrative Health
- Gobierno
- NCCIH NIH HHS
- Subvenciones
- National Natural Science Foundation of China (2015225); National Natural Science Foundation of China (81671378); National Natural Science Foundation of China (1-15-BS-018); National Natural Science Foundation of China (81470495); National Natural Science Foundation of China (2015203); National Natural Science Foundation of China (81370318); National Natural Science Foundation of China (81570344); National Center for Complementary and Integrative Health (P01 AT003961); Jilin University (2015225); Jilin University (2015203); Jilin University (81273509); National Natural Science Foundation of China (81300186); National Natural Science Foundation of China (81273509); American Diabetes Association (1–15-BS-018); American Diabetes Association (81273509); National Natural Science Foundation of China (81400281); American Diabetes Association (81370318); National Natural Science Foundation of China (81470061); Jilin University (81570344)
Según 5 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2018-01-02 · Redox Biol · vol. 15 · págs. 405–417
- Editorial
- Elsevier BV
- Citado
- 182 citas · más que el 98% de estudios similares · 6.8× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 43 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY-NC-ND
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Protein Tyrosine Phosphatases · Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Palabras clave
- FYN, Sulforaphane, Cardiomyopathy, Angiotensin II, Protein kinase B, Diabetic cardiomyopathy, Chemistry, Activator (genetics), Endocrinology, GSK3B, Internal medicine, Oxidative stress, GSK-3, Cancer research, Phosphorylation, Heart failure, Biology, Medicine, Biochemistry, Gene, Receptor, Proto-oncogene tyrosine-protein kinase Src
- MeSH
- heart, animals, mice, knockout, humans, disease models, animal, isothiocyanates, sulfoxides, angiotensin ii, signal transduction, oxidative stress, male, proto-oncogene proteins c-akt, proto-oncogene proteins c-fyn, nf-e2-related factor 2, phosphatidylinositol 3-kinases, diabetic cardiomyopathies, glycogen synthase kinase 3 beta
10 autores
- Ying Xin🇨🇳🇺🇸Ministry of Education of the People's Republic of China; University of Louisville; Jilin University; Wenzhou Medical University
- Yang Bai🇺🇸🇨🇳University of Louisville; Jilin University; First Hospital of Jilin University
- Xin Mei Jiang🇺🇸🇨🇳University of Louisville; Jilin University; First Hospital of Jilin University
- Shanshan Zhou🇺🇸🇨🇳University of Louisville; Jilin University; First Hospital of Jilin University
- Yuehui Wang🇨🇳Jilin University; First Hospital of Jilin University
- Kupper A. Wintergerst🇺🇸University of Louisville; Kosair Children's Hospital; Diabetes Care Center; Norton Hospital; University of Louisville Hospital
- Taixing Cui🇺🇸University of South Carolina
- Honglei Ji🇨🇳 · autor de correspondenciaJilin University; First Hospital of Jilin University
- Yi Tan🇺🇸🇨🇳 · autor de correspondenciaUniversity of Louisville; Wenzhou Medical University; Diabetes Care Center
- Lu Cai🇺🇸🇨🇳University of Louisville; Wenzhou Medical University; Diabetes Care Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
Aims
Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) by sulforaphane (SFN) protects from, and deletion of the Nrf2 gene exaggerates, diabetic cardiomyopathy. Angiotensin II (Ang II) plays a critical role in the development of diabetic cardiomyopathy. Therefore, whether SFN prevents Ang II-induced cardiomyopathy through activation of Nrf2 was examined using wild-type, global deletion of Nrf2 gene (Nrf2-KO) and cardiomyocyte-specific overexpression of Nrf2 gene (Nrf2-TG) mice.
Methods and results
Administration of a subpressor dose of Ang II to wild-type mice induced cardiac oxidative stress, inflammation, remodeling and dysfunction, all of which could be prevented by SFN treatment with Nrf2 up-regulation and activation. Nrf2-KO mice are susceptible, and Nrf2-TG mice are resistant, respectively, to Ang II-induced cardiomyopathy. Meanwhile, the ability of SFN to protect against Ang II-induced cardiac damage was lost in Nrf2-KO mice. Up-regulation and activation of Nrf2 by SFN is accompanied by activation of Akt, inhibition of glycogen synthase kinase (GSK)-3β, and accumulation of Fyn in nuclei. In vitro up-regulation of Nrf2 by SFN was abolished and nuclear Fyn accumulation was increased when cardiac cells were exposed to a PI3K inhibitor or GSK-3β-specific activator.
Conclusion
These results suggest that Nrf2 plays a central role in the prevention of Ang II-induced cardiomyopathy, and SFN prevents Ang II-induced cardiomyopathy partially via the Akt/GSK-3β/Fyn-mediated Nrf2 activation.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC-ND).
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