Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

Jovanović, Aleksandra; Obradović, Milan; Sudar-Milovanović, Emina; Stewart, Alan J.; Pitt, Samantha J.; Alavantić, Dragan; Aleksic, Ema; Isenović, Esma R.

doi:10.1007/s11010-017-3077-y

Cited by 3 publications

(2 citation statements)

References 72 publications

(88 reference statements)

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“…However, ROCK2 also phosphorylates cardiac troponin I (cTnI) and troponin T (cTnT) and inhibits the troponin complex, thus reducing the Ca 2+ -elicited development of tension [ 39 , 81 ]. The activation of ROCK under mechanical or metabolic stress promotes the function of sarcolemma proteins involved in cardiac action potential propagation and the generation of intracellular Ca 2+ transients [ 83 , 84 , 85 , 86 , 87 ]. Therefore, ROCK inhibition may represent a strategy not only for limiting the progression of heart failure but also for controlling the development of arrhythmias.…”

Section: Cellular Effects Of Rock On the Cardiovascular Systemmentioning

confidence: 99%

ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

Montagnoli

Sudo

et al. 2021

Cells

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Pulmonary hypertension (PH) is a cardiovascular disease caused by extensive vascular remodeling in the lungs, which ultimately leads to death in consequence of right ventricle (RV) failure. While current drugs for PH therapy address the sustained vasoconstriction, no agent effectively targets vascular cell proliferation and tissue inflammation. Rho-associated protein kinases (ROCKs) emerged in the last few decades as promising targets for PH therapy, since ROCK inhibitors demonstrated significant anti-remodeling and anti-inflammatory effects. In this review, current aspects of ROCK inhibition therapy are discussed in relation to the treatment of PH and RV dysfunction, from cell biology to preclinical and clinical studies.

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Section: Cellular Effects Of Rock On the Cardiovascular Systemmentioning

confidence: 99%

ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

Montagnoli

Sudo

et al. 2021

Cells

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“…3 Decreased NKA activity and expression were also found in the hearts of mammals following myocardial infarction, obesity, insulin resistance, diabetes, and hypertension. [4][5][6] The regulation of NKA activity and expression could be important in the treatment of cardio-diseases.…”

Section: Introductionmentioning

confidence: 99%

Na⁺/K⁺-ATPase DR region antibody ameliorated cardiac hypertrophy and fibrosis in rats with 5/6 nephrectomy

Zheng

Lan

Meng

et al. 2022

Exp Biol Med (Maywood)

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The enzyme Na+/K+-ATPase (NKA) is important in the heart. Reductions in NKA activity and expression have often been observed in chronic kidney disease (CKD)-related heart injury. Previously, our group found that an antibody targeting the NKA1α1 subunit’s DR extracellular region (897DVEDSYGQQWTYEQR911) stimulated NKA activities and produced cardioprotective effects against ischemic injury and isoproterenol-induced cardiac remodeling. In here, we assessed whether DRm217, a specific DR antibody, exhibits cardioprotective effects in chronic renal failure models. In 5/6 nephrectomy (5/6 Nx) surgery to mimic CKD in Sprague Dawley rat, we observed that NKA activity and expression were depressed in the hearts of 5/6 Nx rats. DRm217, an NKA DR region antibody, alleviated heart hypertrophy and cardiac fibrosis under 5/6 Nx conditions. Further studies revealed that DRm217 inhibited Src activation and reduced reactive oxygen species (ROS) levels in hearts under 5/6 Nx conditions. Our findings imply that NKA could be a treatment target in CKD-related cardiac diseases. Prevention of CKD-induced myocardial injury by DRm217 provides an appealing therapeutic alternative.

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Regulation of Na+-K+-ATPase leads to disturbances of isoproterenol-induced cardiac dysfunction via interference of Ca2+-dependent cardiac metabolism

Yan,

Li,

Lan

et al. 2024

Clinical Science

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Reductions in Na+-K+-ATPase (NKA) activity and expression are often observed in the progress of various reason-induced heart failure (HF). However, NKA α1 mutation or knockdown cannot cause spontaneous heart disease. Whether the abnormal NKAα1 directly contributes to HF pathogenesis remains unknown. Here, we challenge NKA α1 +/- mice with isoproterenol to evaluate the role of NKA α1 haploinsufficiency in isoproterenol (ISO)-induced cardiac dysfunction. Genetic knockdown of NKAα1 accelerated ISO-induced cardiac cell hypertrophy, heart fibrosis, and dysfunction. Further studies revealed decreased Krebs cycle, fatty acid oxidation, and mitochondrial OXPHOS in the hearts of NKA α1 +/- mice challenged with ISO. In ISO-treated conditions, inhibition of NKA elevated cytosolic Na+, further reduced mitochondrial Ca2+ via mNCE, and then finally downregulated cardiac cell energy metabolism. In addition, a supplement of DRm217 alleviated ISO-induced heart dysfunction, mitigated cardiac remodeling, and improved cytosolic Na+ and Ca2+ elevation and mitochondrial Ca2+ depression in the NKAα1+/− mouse model. The findings suggest that targeting NKA and mitochondria Ca2+ could be a promising strategy in the treatment of heart disease.

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Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

Abstract: The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high fat (HF) diet on activity/expression of the cardiac Na + /K + -ATPase, via

Cited by 3 publications

References 72 publications

ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

Na⁺/K⁺-ATPase DR region antibody ameliorated cardiac hypertrophy and fibrosis in rats with 5/6 nephrectomy

Regulation of Na+-K+-ATPase leads to disturbances of isoproterenol-induced cardiac dysfunction via interference of Ca2+-dependent cardiac metabolism

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Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

Abstract: The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high fat (HF) diet on activity/expression of the cardiac Na + /K + -ATPase, via

Cited by 3 publications

References 72 publications

ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

ROCK Inhibition as Potential Target for Treatment of Pulmonary Hypertension

Na+/K+-ATPase DR region antibody ameliorated cardiac hypertrophy and fibrosis in rats with 5/6 nephrectomy

Regulation of Na+-K+-ATPase leads to disturbances of isoproterenol-induced cardiac dysfunction via interference of Ca2+-dependent cardiac metabolism

Contact Info

Product

Resources

About

Na⁺/K⁺-ATPase DR region antibody ameliorated cardiac hypertrophy and fibrosis in rats with 5/6 nephrectomy