9/14/2023 0 Comments M6a dot blot protocol![]() ![]() Even in the clinic, oral administration of a low dose (50 or 100 mg/day) for systemic sclerosis or lupus erythematosus for 1 week has caused cardiac electrical alteration (prolonged QT interval) in some patients. Further, CYP is widely used in the treatment of other diseases, such as refractory neuromyelitis optica spectrum disorder (200 mg/kg) ( 6) and rapidly progressive systemic sclerosis (300 mg/kg) ( 7), all of reportedly cause severe cardiotoxicity. Up to 28% of patients who received a high dose of CYP suffered from cardiac arrhythmias ( 3) and even heart failure ( 5). One traditional antineoplastic agent, cyclophosphamide (CYP), is employed in the treatment of various cancers, including breast, lymphoid, and hematologic malignancies ( 4). Both conventional chemotherapies and targeted drug therapies reportedly induce cardiovascular toxicity events. Many countries and regions have issued relevant practice guidelines for cardiovascular toxicity induced by cancer treatments ( 3). Tumor therapy-induced cardiotoxicity as a common side effect has received increasing attention. Our results revealed a novel mechanism for m6A methylation-dependent regulation of JPH2, which provides new strategies for the treatment and prevention of CYP-induced cardiotoxicity.Īlthough improved treatments have been effective in increasing the survival of patients with tumors, an increase in the number of side effects of cancer treatment have led to mortality ( 1, 2). Importantly, our results demonstrated that CYP induced an increase in the m6A level of JPH2 mRNA by upregulating methyltransferases METT元, leading to the reduction of JPH2 expression levels, as well as increased field potential duration and action potential duration in cardiomyocytes. Moreover, N6-methyladenosine (m6A) methylation sequencing and RNA sequencing suggested that CYP induced cardiotoxicity by dysregulating calcium signaling. Our data demonstrated that CYP-induced a prolonged cardiac QT interval and electromechanical coupling time courses accompanied by JPH2 downregulation. In this study, we used cell and animal models to investigate the effect of CYP on cardiomyocytes. Although it has received significant attention, the related mechanisms of CYP-induced cardiotoxicity remain largely unknown. Cyclophosphamide (CYP)-induced cardiotoxicity is a common side effect of cancer treatment. ![]()
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