Is There a Mitochondrial Protection via Remote Ischemic Conditioning in Settings of Anticancer Therapy Cardiotoxicity?

被引:3
作者
Kleinbongard, Petra [1 ]
Andreadou, Ioanna [2 ]
机构
[1] Univ Essen Gesamthsch, West German Heart & Vasc Ctr, Inst Pathophysiol, Med Sch, Essen, Germany
[2] Natl & Kapodistrian Univ Athens, Fac Pharm, Lab Pharmacol, Athens, Greece
关键词
Anthracycline; Cancer-treatment; Cardioprotection; Cardiotoxicity; Mitochondria; Remote ischemic conditioning; ELEVATION MYOCARDIAL-INFARCTION; ARTERY-BYPASS SURGERY; PRECONDITIONING PRESERVES; SIGNAL-TRANSDUCTION; CLINICAL-OUTCOMES; CARDIOPROTECTION; DOXORUBICIN; PROTEIN; METABOLISM; INHIBITION;
D O I
10.1007/s11897-024-00658-w
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of ReviewTo provide an overview of (a) protective effects on mitochondria induced by remote ischemic conditioning (RIC) and (b) mitochondrial damage caused by anticancer therapy. We then discuss the available results of studies on mitochondrial protection via RIC in anticancer therapy-induced cardiotoxicity.Recent FindingsIn three experimental studies in healthy mice and pigs, there was a RIC-mediated protection against anthracycline-induced cardiotoxicity and there was some evidence of improved mitochondrial function with RIC. The RIC-mediated protection was not confirmed in the two available studies in cancer patients. In adult cancer patients, RIC was associated with an adverse outcome. There are no data on mitochondrial function in cancer patients.SummaryStudies in tumor-bearing animals are needed to determine whether RIC does not interfere with the anticancer properties of the drugs and whether RIC actually improves mitochondrial function, ultimately resulting in improved cardiac function.
引用
收藏
页码:292 / 304
页数:13
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