2019
DOI: 10.1016/j.gene.2019.02.053
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Nandrolone administration with or without strenuous exercise increases cardiac fatal genes overexpression, calcium/calmodulin-dependent protein kinaseiiδ, and monoamine oxidase activities and enhances blood pressure in adult wistar rats

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Cited by 10 publications
(12 citation statements)
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“…In our data, the most reported cardiovascular disorders were platelet aggregation disorders and cardiac injuries. Shirpoor and coauthors [ 59 ], through experiments on rats, showed the molecular mechanisms underlying heart hypertrophy: chronic nandrolone treatment with or without strenuous exercise causes a shift in the alpha and beta–myosin heavy chain (α-MHC/β-MHC) isoform expression manifested by elevation of β-MHC mRNA and the ratio of β-MHC mRNA/α-MHC mRNA expression, as well as an increase in the heart tissue of mono-amine oxidase (MAO) and calcium/calmodulin-dependent protein kinase II-δ activities (CaMKII-δ). Moreover, androgens have receptors in the heart and their action directly affects it through coupling directly with nuclear receptors and increasing the expression of mRNA, thus stimulating cardiac protein synthesis resulting in myocardial hypertrophy [ 60 , 61 ].…”
Section: Discussionmentioning
confidence: 99%
“…In our data, the most reported cardiovascular disorders were platelet aggregation disorders and cardiac injuries. Shirpoor and coauthors [ 59 ], through experiments on rats, showed the molecular mechanisms underlying heart hypertrophy: chronic nandrolone treatment with or without strenuous exercise causes a shift in the alpha and beta–myosin heavy chain (α-MHC/β-MHC) isoform expression manifested by elevation of β-MHC mRNA and the ratio of β-MHC mRNA/α-MHC mRNA expression, as well as an increase in the heart tissue of mono-amine oxidase (MAO) and calcium/calmodulin-dependent protein kinase II-δ activities (CaMKII-δ). Moreover, androgens have receptors in the heart and their action directly affects it through coupling directly with nuclear receptors and increasing the expression of mRNA, thus stimulating cardiac protein synthesis resulting in myocardial hypertrophy [ 60 , 61 ].…”
Section: Discussionmentioning
confidence: 99%
“…They found that swimming training combined with high doses of nandrolone (5 mg/kg per injection, equal to 10 mg/kg per week) aggravates cardiac hypertrophy with interstitial fibrosis. A recent study showed that chronic nandrolone treatment with or without severe training causes a significant increase in beta-myosin heavy chain (β-MHC) gene expression, calcium/calmodulin-dependent protein kinase II (CaMKII), and monoamine oxidase (MAO) activities in the heart tissue of male Wistar rats [79].…”
Section: Discussionmentioning
confidence: 99%
“…More importantly, in AAS use, hypogonadism and depression are durable side effects that prevent the user from refraining in its use. Furthermore, it is possible that despite discontinuation, there may be permanent changes from AASs that includes insulin resistance, hypertension and visceral adipose tissue [60].…”
Section: Discussionmentioning
confidence: 99%
“…This includes overexpression of calcium/calmodulin dependent protein kinase II delta (CaMKIIδ), beta myosin heavy chain (MHC) and monoamine oxidase (MAO), hallmarks of pathological changes within the myocardium, such as myocyte apoptosis, cardiac hypertrophy, slow shortening velocity of cardiac fibres and arrhythmias [60]. More significantly, imbalance of Ca 2+ homeostasis and increased CaMKIIδ activity is observed in both human and animal models of heart failure [60]. The overproduction of MAO is also related to ventricular dysfunction, apoptosis and fibrosis [60].…”
Section: Aass Geneticsmentioning
confidence: 99%
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