Umbilical cord blood-mesenchymal stem cells and carvedilol reduce doxorubicin- induced cardiotoxicity: Possible role of insulin-like growth factor-1

Mousa, Hanaa S.E.; Aal, Sara M. Abdel; Abbas, Noha

doi:10.1016/j.biopha.2018.06.051

Cited by 15 publications

(7 citation statements)

References 55 publications

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“…Apart from that, exogenous IGF-1 (81) or insulin (82) were reported to alleviated DOX-induced cardiomyocyte apoptosis via stimulating PI3K-AKT. Interestingly, Mousa et al discovered that the co-treatment of human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) and carvedilol alleviated DOX-induced decrease of cardiac muscle fiber diameter, which is accompanied with the elevation of IGF-1, GATA-binding protein 4 (GATA-4), and vascular endothelial growth factor (VEGF) (83). Studies have uncovered that IGF-1 is a pro-hypertrophic inducer in cardiomyocyte (84,85).…”

Section: Phosphoinositide 3-kinase (Pi3k)mentioning

confidence: 99%

Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity

Chen

Yan

Yang

2022

Front. Cardiovasc. Med.

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Left ventricular (LV) mass loss is prevalent in doxorubicin (DOX)-induced cardiotoxicity and is responsible for the progressive decline of cardiac function. Comparing with the well-studied role of cell death, the part of cardiomyocyte atrophy (CMA) playing in the LV mass loss is underestimated and the knowledge of the underlying mechanism is still limited. In this review, we summarized the recent advances in the DOX-induced CMA. We found that the CMA caused by DOX is associated with the upregulation of FOXOs and “atrogenes,” the activation of transient receptor potential canonical 3-NADPH oxidase 2 (TRPC3-Nox2) axis, and the suppression of IGF-1-PI3K signaling pathway. The imbalance of anabolic and catabolic process may be the common final pathway of these mechanisms. At last, we provided some strategies that have been demonstrated to alleviate the DOX-induced CMA in animal models.

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Section: Phosphoinositide 3-kinase (Pi3k)mentioning

confidence: 99%

Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity

Chen

Yan

Yang

2022

Front. Cardiovasc. Med.

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“…The bone marrow, adipose tissue, and umbilical cord blood are the most common sites for MSC extraction. The most commonly used cells in the reviewed studies were BMMSCs (Chen et al, 2006; Garbade et al, 2009; Mohammadi Gorji et al, 2012; Yu et al, 2014; Ammar et al, 2015; Dias et al, 2015; Deng et al, 2017; Soliman et al, 2017; Zeng et al, 2017) and human umbilical cord blood (hUCB)-MSCs (Gopinath et al, 2010; Di et al, 2012; Abd Allah and Hussein, 2017; Mao et al, 2017; Mousa et al, 2018). Fewer studies used adipose-derived stem cells (ADSCs) (Oliveira et al, 2013; Pınarlı et al, 2013) and fetal-derived stem cells (Haydardedeoglu et al, 2018).…”

Section: Factors That Influence the Outcome Of Msc Therapy For Dox Camentioning

confidence: 99%

“…Mousa et al reported that the combination of hUCB-MSCs and carvedilol reduced DOX-induced electrocardiographic abnormalities and cardiac concentrations of oxidative stress markers and caspase-3. This may be due to its antioxidant and anti-inflammatory effects (Mousa et al, 2018). DOX has been reported to induce oxidative stress and senescence in MSCs (Xia and Hou, 2018b; Kozhukharova et al, 2018).…”

Section: Factors That Influence the Outcome Of Msc Therapy For Dox Camentioning

confidence: 99%

Mesenchymal Stem Cell Therapy for Doxorubicin-Induced Cardiomyopathy: Potential Mechanisms, Governing Factors, and Implications of the Heart Stem Cell Debate

et al. 2019

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Over the past decades, researchers have reported several mechanisms for doxorubicin (DOX)-induced cardiomyopathy, including oxidative stress, inflammation, and apoptosis. Another mechanism that has been suggested is that DOX interferes with the cell cycle and induces oxidative stress in C-kit+ cells (commonly known as cardiac progenitor cells), reducing their regenerative capacity. Cardiac regeneration through enhancing the regenerative capacity of these cells or administration of other stem cells types has been the axis of several studies over the past 20 years. Several experiments revealed that local or systemic injections with mesenchymal stem cells (MSCs) were associated with significantly improved cardiac function, ameliorated inflammatory response, and reduced myocardial fibrosis. They also showed that several factors can affect the outcome of MSC treatment for DOX cardiomyopathy, including the MSC type, dose, route, and timing of administration. However, there is growing evidence that the C-kit+ cells do not have a cardiac regenerative potential in the adult mammalian heart. Similarly, the protective mechanisms of MSCs against DOX-induced cardiomyopathy are not likely to include direct differentiation into cardiomyocytes and probably occur through paracrine secretion, antioxidant and anti-inflammatory effects. Better understanding of the involved mechanisms and the factors governing the outcomes of MSCs therapy are essential before moving to clinical application in patients with DOX-induced cardiomyopathy.

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“…Determination of apoptosis pathways has been reported to be one of the most effective methods of detecting Dox-IC (12). Following DOX administration, oxidative stress occurs due to increased levels of reactive oxygen species and free oxygen radicals, particularly intracellular calcium, in myofibers and endothelial cells in the heart, causing necrosis and apoptosis in cardiomyocytes (22).…”

Section: Resultsmentioning

confidence: 99%

Cardioprotective effects of fetal kidney-derived mesenchymal stem cells on doxorubicin-induced cardiotoxicity in rats

Yavuz¹,

Özgermen²,

Haydardedeoğlu³

et al. 2022

Medycyna Weterynaryjna

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Cardiotoxicity is one of the most common side effects of doxorubicin (DOX), a chemotherapy drug used in the treatment of many carcinomas. In recent years, stem-cell therapies have been successfully used to prevent cardiotoxicity. This study investigated the efficacy of intraperitoneally administered fetal kidney-derived mesenchymal stem cells (FKD-MSCs) in preventing DOX-induced cardiotoxicity in rats. For this purpose, thirty rats were randomly divided into three groups: control, DOX and mesenchymal stem cell (MSC) groups. Adriamycin was injected as a single dose via the tail vein in the DOX and MSC groups in order to induce cardiotoxicity. FKD-MSC was applied to the MSC group by the intraperitoneal route after cardiotoxicity had been established. Then the rats were euthanized, and routine histological procedures were performed on their hearts. H&E and Masson’s stains were used for histopathology. Cardiac Troponin-T and I (cTnT, cTnI), Caspase-3 and BCL-XL antibodies were used for immunohistochemistry. Vacuoles, edema, degeneration and necrosis were observed histopathologically mostly in the DOX group. Lesions in the control and MSC groups were less severe. Fibrosis in the control and MSC groups was milder. cTnT and cTnI immunopositive staining was most commonly seen in the control group, followed by the MSC group. Immunohistochemical staining by Caspase-3 and BCL-XL showed that their expressions in the MSC group were statistically similar to those in the control group. Accordingly, it was concluded that the intraperitoneal application of MSC had a positive effect on histopathological findings, fibrosis, immunohistochemistry, especially apoptosis, neovascularization, and anti-apoptotic development, whereas troponin levels were not found to be therapeutic.

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Umbilical cord blood-mesenchymal stem cells and carvedilol reduce doxorubicin- induced cardiotoxicity: Possible role of insulin-like growth factor-1

Cited by 15 publications

References 55 publications

Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity

Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity

Mesenchymal Stem Cell Therapy for Doxorubicin-Induced Cardiomyopathy: Potential Mechanisms, Governing Factors, and Implications of the Heart Stem Cell Debate

Cardioprotective effects of fetal kidney-derived mesenchymal stem cells on doxorubicin-induced cardiotoxicity in rats

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