Evidence for cardiac atrophic remodeling in cancer-induced cachexia in mice

Tian, Min; Michelle, L.; Nishijima, Yoshinori; Belury, Martha A.

doi:10.3892/ijo.2011.1150

Cited by 45 publications

(47 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cancer cachexia, a syndrome consisting of fatigue, muscle wasting, and weight loss with or without anorexia, is observed in a large percentage of cancer patients with incurable disease [1] and contributes to 22 percent of cancer deaths [1, 2]. New research by our lab and others has shown that cancer cachexia involves not only the loss of skeletal muscle, but can also cause pathologic alterations within the heart [2, 3].…”

Section: Introductionmentioning

confidence: 99%

“…New research by our lab and others has shown that cancer cachexia involves not only the loss of skeletal muscle, but can also cause pathologic alterations within the heart [2, 3]. The resultant effects on myocardial function likely contribute to fatigue and decreased quality of life in these patients.…”

Section: Introductionmentioning

confidence: 99%

“…We and others have demonstrated tumor-induced cardiac remodeling and myocardial dysfunction [2–4]. Tumor-induced cardiac remodeling involves increased expression of pro-inflammatory cytokines, such as interleukin-6 (IL-6) [5], as well as ventricular wall thinning and decreased troponin I levels (a protein involved in cardiac contraction) [2].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Losartan treatment attenuates tumor-induced myocardial dysfunction

Stevens

Velten²,

Youtz

et al. 2015

Journal of Molecular and Cellular Cardiology

View full text Add to dashboard Cite

Fatigue and muscle wasting are common symptoms experienced by cancer patients. Data from animal models demonstrate that angiotensin is involved in tumor-induced muscle wasting, and that tumor growth can independently affect myocardial function, which could contribute to fatigue in cancer patients. In clinical studies, inhibitors of angiotensin converting enzyme (ACE) can prevent the development of chemotherapy-induced cardiovascular dysfunction, suggesting a mechanistic role for the renin-angiotensin-aldosterone system (RAAS). In the present study, we investigated whether an angiotensin (AT)1-receptor antagonist could prevent the development of tumor-associated myocardial dysfunction. Methods and Results: Colon26 adenocarcinoma (c26) cells were implanted into female CD2F1 mice at 8 weeks of age. Simultaneously, mice were administered Losartan (10 mg/kg) daily via their drinking water. In vivo echocardiography, blood pressure, in vitro cardiomyocyte function, cell proliferation assays, and measures of systemic inflammation and myocardial protein degradation were performed 19 days following tumor cell injection. Losartan treatment prevented tumor-induced loss of muscle mass and in vitro c26 cell proliferation, decreased tumor weight, and attenuated myocardial expression of interleukin-6. Furthermore, Losartan treatment mitigated tumor-associated alterations in calcium signaling in cardiomyocytes, which was associated with improved myocyte contraction velocity, systolic function, and blood pressures in the hearts of tumor-bearing mice. Conclusions: These data suggest that Losartan may mitigate tumor-induced myocardial dysfunction and inflammation.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Losartan treatment attenuates tumor-induced myocardial dysfunction

Stevens

Velten²,

Youtz

et al. 2015

Journal of Molecular and Cellular Cardiology

View full text Add to dashboard Cite

show abstract

“…The pathogenesis of cardiac atrophy remains poorly explored but seems to share similar mechanisms with skeletal muscle atrophy. Indeed, reduced protein synthesis and increased protein degradation in hearts of cachectic rodents were detected [33,34]. In addition, cardiomyocytes apoptosis was also observed in AH-130 tumour-bearing rats and C26 tumour bearing mice cachectic models [35,36].…”

Section: Cancer Cachexiamentioning

confidence: 99%

mTOR and Tumor Cachexia

Duval

Jeanneret

Santoro

et al. 2018

IJMS

View full text Add to dashboard Cite

Cancer cachexia affects most patients with advanced forms of cancers. It is mainly characterized by weight loss, due to muscle and adipose mass depletion. As cachexia is associated with increased morbidity and mortality in cancer patients, identifying the underlying mechanisms leading to cachexia is essential in order to design novel therapeutic strategies. The mechanistic target of rapamycin (mTOR) is a major intracellular signalling intermediary that participates in cell growth by upregulating anabolic processes such as protein and lipid synthesis. Accordingly, emerging evidence suggests that mTOR and mTOR inhibitors influence cancer cachexia. Here, we review the role of mTOR in cellular processes involved in cancer cachexia and highlight the studies supporting the contribution of mTOR in cancer cachexia.

show abstract

“…Pathologic insults were demonstrated by showing that tumor-bearing mice presented with reduced levels of PPAR-α and carnitine palmitoyltransferase (CPT1β), compared to those without tumors (Tian et al, 2011). This phenomenon suggested that pathological hypertrophy occurs through the down regulation of fatty acid metabolism.…”

Section: Introductionmentioning

confidence: 99%

In vitro effects of exercise on the heart

et al. 2014

View full text Add to dashboard Cite

Pathologic and physiologic factors acting on the heart can produce consistent pressure changes, volume overload, or increased cardiac output. These changes may then lead to cardiac remodeling, ultimately resulting in cardiac hypertrophy. Exercise can also induce hypertrophy, primarily physiologic in nature. To determine the mechanisms responsible for each type of remodeling, it is important to examine the heart at the functional unit, the cardiomyocyte. Tests of individual cardiomyocyte function in vitro provide deeper understanding of the changes occurring within the heart during hypertrophy. Examination of cardiomyocyte function during exercise primarily follows one of two pathways: the addition of hypertrophic inducing agents in vitro to normal cardiomyocytes, or the use of trained animal models and isolating cells following the development of hypertrophy in vivo. Due to the short lifespan of adult cardiomyocytes, a proportionately scant amount of research exists involving the direct stimulation of cells in vitro to induce hypertrophy. These attempts provide the only current evidence, as it is difficult to gather extensive data demonstrating cell growth as a result of in vitro physical stimulation. Researchers have created ways to combine skeletal myocytes with cardiomyocytes to produce functional muscle cells used to repair pathologic heart tissue, but continue to struggle with the short lifespan of these cells. While there have been promising findings regarding the mechanisms that surround cardiac hypertrophy in vitro, the translation of in vitro findings to in vivo function is not consistent. Therefore, the focus of this review is to highlight recent studies that have investigated the effect of exercise on the heart, both in vitro and in vivo.

show abstract

Evidence for cardiac atrophic remodeling in cancer-induced cachexia in mice

Cited by 45 publications

References 0 publications

Losartan treatment attenuates tumor-induced myocardial dysfunction

Losartan treatment attenuates tumor-induced myocardial dysfunction

mTOR and Tumor Cachexia

In vitro effects of exercise on the heart

Contact Info

Product

Resources

About