Nonclassical Axis of the Renin-Angiotensin System and Neprilysin: Key Mediators That Underlie the Cardioprotective Effect of PPAR-Alpha Activation during Myocardial Ischemia in a Metabolic Syndrome Model
Joint Authors
Rubio-Ruiz, M. E.
Sánchez-Aguilar, María
Ibarra-Lara, Luz
del Valle-Mondragón, Leonardo
Soria-Castro, Elizabeth
Torres-Narváez, Juan Carlos
Carreón-Torres, Elizabeth
Sánchez-Mendoza, Alicia
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-11-28
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
The activation of the renin-angiotensin system (RAS) participates in the development of metabolic syndrome (MetS) and in heart failure.
PPAR-alpha activation by fenofibrate reverts some of the effects caused by these pathologies.
Recently, nonclassical RAS components have been implicated in the pathogenesis of hypertension and myocardial dysfunction; however, their cardiac functions are still controversial.
We evaluated if the nonclassical RAS signaling pathways, directed by angiotensin III and angiotensin-(1-7), are involved in the cardioprotective effect of fenofibrate during ischemia in MetS rats.
Control (CT) and MetS rats were divided into the following groups: (a) sham, (b) vehicle-treated myocardial infarction (MI-V), and (c) fenofibrate-treated myocardial infarction (MI-F).
Angiotensin III and angiotensin IV levels and insulin increased the aminopeptidase (IRAP) expression and decreased the angiotensin-converting enzyme 2 (ACE2) expression in the hearts from MetS rats.
Ischemia activated the angiotensin-converting enzyme (ACE)/angiotensin II/angiotensin receptor 1 (AT1R) and angiotensin III/angiotensin IV/angiotensin receptor 4 (AT4R)-IRAP axes.
Fenofibrate treatment prevented the damage due to ischemia in MetS rats by favoring the angiotensin-(1-7)/angiotensin receptor 2 (AT2R) axis and inhibiting the angiotensin III/angiotensin IV/AT4R-IRAP signaling pathway.
Additionally, fenofibrate downregulated neprilysin expression and increased bradykinin production.
These effects of PPAR-alpha activation were accompanied by a reduction in the size of the myocardial infarct and in the activity of serum creatine kinase.
Thus, the regulation of the nonclassical axis of RAS forms part of a novel protective effect of fenofibrate in myocardial ischemia.
American Psychological Association (APA)
Sánchez-Aguilar, María& Ibarra-Lara, Luz& del Valle-Mondragón, Leonardo& Soria-Castro, Elizabeth& Torres-Narváez, Juan Carlos& Carreón-Torres, Elizabeth…[et al.]. 2020. Nonclassical Axis of the Renin-Angiotensin System and Neprilysin: Key Mediators That Underlie the Cardioprotective Effect of PPAR-Alpha Activation during Myocardial Ischemia in a Metabolic Syndrome Model. PPAR Research،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1206648
Modern Language Association (MLA)
Sánchez-Aguilar, María…[et al.]. Nonclassical Axis of the Renin-Angiotensin System and Neprilysin: Key Mediators That Underlie the Cardioprotective Effect of PPAR-Alpha Activation during Myocardial Ischemia in a Metabolic Syndrome Model. PPAR Research No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1206648
American Medical Association (AMA)
Sánchez-Aguilar, María& Ibarra-Lara, Luz& del Valle-Mondragón, Leonardo& Soria-Castro, Elizabeth& Torres-Narváez, Juan Carlos& Carreón-Torres, Elizabeth…[et al.]. Nonclassical Axis of the Renin-Angiotensin System and Neprilysin: Key Mediators That Underlie the Cardioprotective Effect of PPAR-Alpha Activation during Myocardial Ischemia in a Metabolic Syndrome Model. PPAR Research. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1206648
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1206648