The role of microtubules in structural remodeling and the progression to heart failure

Roos, Kenneth P.; Palmer, R. E.; Miller, T. W.

doi:10.1054/jcaf.2002.129281

Cited by 13 publications

(8 citation statements)

References 42 publications

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“…In this experiment, the level of beta‐tubulin was reduced in the LV of isoproterenol‐treated rats, while melatonin administration partly prevented the alteration of beta‐tubulin. Although the biological impact of changes in cytoarchitecture is not unequivocally clear and seems to depend upon an experimental model and conditions , the alteration of tubulin level reflects the altered microtubule structure and the inhibition of these changes may be considered as favorable. Partial prevention of fibrosis and alterations in cytoarchitecture by melatonin reflects the tendency of this indolamine to preserve the physiologic structure of the myocardium, exerting a potentially beneficial impact on the heart function and prognosis.…”

Section: Discussionmentioning

confidence: 99%

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol‐induced heart failure

Šimko

Bednarova

Krajcirovicova

et al. 2014

Journal of Pineal Research

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Melatonin was previously shown to reduce blood pressure and left ventricular (LV) remodeling in several models of experimental heart damage. This study investigated whether melatonin prevents LV remodeling and improves survival in isoproterenol-induced heart failure. In the first experiment, four groups of 3-month-old male Wistar rats (12 per group) were treated for 2 wk as follows: controls, rats treated with melatonin (10 mg/kg/day) (M), rats treated with isoproterenol (5 mg/kg/day intraperitoneally the second week) (Iso), and rats treated with melatonin (2 wk) and isoproterenol (the second week) in corresponding doses (IsoM). In the second experiment, 30 rats were treated with isoproterenol and 30 rats with isoproterenol plus melatonin for a period of 28 days and their mortality was investigated. Isoproterenol-induced heart failure with hypertrophy of the left and right ventricles (LV, RV), lowered systolic blood pressure (SBP) and elevated pulmonary congestion. Fibrotic rebuilding was accompanied by alterations of tubulin level in the LV and oxidative stress development. Melatonin failed to reduce the weight of the LV or RV; however, it curtailed the weight of the lungs and attenuated the decline in SBP. Moreover, melatonin decreased the level of oxidative stress and of insoluble and total collagen and partly prevented the beta-tubulin alteration in the LV. Most importantly, melatonin reduced mortality and prolonged the average survival time. In conclusion, melatonin exerts cardioprotective effects and improves outcome in a model of isoproterenol-induced heart damage. The antiremodeling effect of melatonin may be of potential benefit in patients with heart failure.

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Section: Discussionmentioning

confidence: 99%

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol‐induced heart failure

Šimko

Bednarova

Krajcirovicova

et al. 2014

Journal of Pineal Research

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“…79,81,82 Paclitaxel, similar to colchicine, is microtubule-stabilizing agent, and in normal postmitotic cardiomyocytes, microtubule density is low; thus, taxane agents are not thought to hinder cardiomyocyte contraction. 83 However, small clinical trial data demonstrate that taxane exposure may contribute to LV dysfunction. 76,84 A preclinical investigation of paclitaxel exposure alone versus in conjunction with trastuzumab identified that concomitant inhibition of ERBB2 receptors and paclitaxel treatment has an additive worsening effect on adult cardiomyocytes, mainly discernible in changes of myofibrillar structure and function, but not causing myocyte cell death.…”

Section: Microtubule Inhibitorsmentioning

confidence: 99%

Cardio-Oncology

Lenneman

Sawyer

2016

Circulation Research

348

138

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Through the success of basic and disease-specific research, cancer survivors are one of the largest growing subsets of individuals accessing the healthcare system. Interestingly, cardiovascular disease is the second leading cause of morbidity and mortality in cancer survivors after recurrent malignancy. This recognition has helped stimulate a collaboration between oncology and cardiology practitioners and researchers, and the portmanteau cardio-oncology (also known as onco-cardiology) can now be found in many medical centers. This collaboration promises new insights into how cancer therapies impact cardiovascular homeostasis and long-term effects on cancer survivors. In this review, we will discuss the most recent views on the cardiotoxicity related to various classes of chemotherapy agents and radiation. We will also discuss broadly the current strategies for treating and preventing cardiovascular effects of cancer therapy.

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“…Most of the previous work has focused on pressure-overload LV hypertrophy and shown that microtubule upregulation may be one of the underlying mechanisms responsible for reduced contractility leading to heart failure. 10,[21][22][23][24] The ␣-tubulins in chronic heart failure undergo posttranslational modifications involving detyrosinated Glu-tubulin and deglutamylated delta2-tubulin. 10 The thought is that these changes enhance the stability of the microtubule network, leading to increased stiffness in the left ventricle.…”

Section: Microtubulinmentioning

confidence: 99%

Pretreatment With Angiotensin Receptor Blockade Prevents Left Ventricular Dysfunction and Blunts Left Ventricular Remodeling Associated With Acute Myocardial Infarction

et al. 2006

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The role of microtubules in structural remodeling and the progression to heart failure

Cited by 13 publications

References 42 publications

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol‐induced heart failure

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol‐induced heart failure

Cardio-Oncology

Pretreatment With Angiotensin Receptor Blockade Prevents Left Ventricular Dysfunction and Blunts Left Ventricular Remodeling Associated With Acute Myocardial Infarction

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