2021
DOI: 10.1016/j.abb.2021.108866
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Effect of l-carnitine on cardiotoxicity and apoptosis induced by imatinib through PDGF/ PPARγ /MAPK pathways

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Cited by 17 publications
(9 citation statements)
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“…27,28 Meanwhile, different cell death forms including apoptosis and autophagy have been discovered in IMA-induced cardiotoxicity. 29,30 In our previous research, we found that ferroptosis also participates in IMA-induced cardiotoxicity and the IC 50 value of IMA in H9c2 cells is close to 20 μM, which is reasonable in patients. 25 In agreement with clinical trials on cardiotoxicity, the data showed that the obvious increase in serum LDH and CK levels in mice was partially due to IMA treatment.…”
Section: Discussionmentioning
confidence: 61%
“…27,28 Meanwhile, different cell death forms including apoptosis and autophagy have been discovered in IMA-induced cardiotoxicity. 29,30 In our previous research, we found that ferroptosis also participates in IMA-induced cardiotoxicity and the IC 50 value of IMA in H9c2 cells is close to 20 μM, which is reasonable in patients. 25 In agreement with clinical trials on cardiotoxicity, the data showed that the obvious increase in serum LDH and CK levels in mice was partially due to IMA treatment.…”
Section: Discussionmentioning
confidence: 61%
“…Recent studies have shown that PPAR-gamma is involved in the proliferation of cells in various organs, such as the colon, breast, and bladder; moreover (dys)regulation of PPAR-gamma signaling pathways may participate in tumor occurrence and development in these organs (Lehrke and Lazar, 2005;Yousefnia et al, 2018). Additionally, as a crucial ligand-inducible transcription factor, PPAR-gamma may perform a variety of functions in the mechanisms of some therapeutic drugs (Cheng et al, 2019;Mansour et al, 2021). In early research, it was clear that PPAR-gamma is the dominant regulator of adipogenesis and can modulate metabolism and inflammation in immune cells (Tontonoz and Spiegelman, 2008).…”
Section: Discussionmentioning
confidence: 99%
“…Their adverse events on the cardiovascular system, hypertension, thromboembolism, pulmonary hypertension and ventricular dysfunction are described [42]. Specifically, imatinib, a first-generation tyrosine kinase inhibitor, approved for chronic myeloid leukemia, induces cardiotoxicity altering mitochondrial function through changes within the membrane potential, impairing endoplasmic reticulum response to stress, promoting apoptotic pathways and increasing reactive oxidative species production [43]. The specific mechanism of imatinib-induced cardiotoxicity is through the down-regulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) levels, with a subsequent alteration in carnitine homeostasis, mitochondrial dysfunction and decreased ATP generation [43].…”
Section: Doxorubicin Imatinibmentioning
confidence: 99%
“…Specifically, imatinib, a first-generation tyrosine kinase inhibitor, approved for chronic myeloid leukemia, induces cardiotoxicity altering mitochondrial function through changes within the membrane potential, impairing endoplasmic reticulum response to stress, promoting apoptotic pathways and increasing reactive oxidative species production [43]. The specific mechanism of imatinib-induced cardiotoxicity is through the down-regulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) levels, with a subsequent alteration in carnitine homeostasis, mitochondrial dysfunction and decreased ATP generation [43]. Through the same mechanism, imatinib seems to increase oxidative stress and the production of nitric oxidative species in vessels, thus leading to endothelial dysfunction in vivo [44] (Figure 1).…”
Section: Doxorubicin Imatinibmentioning
confidence: 99%