Mechanisms underlying the cross-talk between heart and cancer

被引：18

作者：

Brancaccio, Mara ^{[1
]}

Pirozzi, Flora ^{[2
]}

Hirsch, Emilio ^{[1
]}

Ghigo, Alessandra ^{[1
]}

机构：

[1] Univ Torino, Dept Mol Biotechnol & Hlth Sci, Mol Biotechnol Ctr, Via Nizza 52, I-10126 Turin, Italy

[2] Univ Naples Federico II, Dept Translat Med Sci, Naples, Italy

来源：

JOURNAL OF PHYSIOLOGY-LONDON | 2020年 / 598卷 / 14期

关键词：

heart failure; cancer; co-morbidities; inflammation; cross-talk; TUMOR-NECROSIS-FACTOR; CLONAL HEMATOPOIESIS; CARDIOVASCULAR-DISEASE; CARDIAC ATROPHY; FACTOR-ALPHA; ACTIVIN-A; DIASTOLIC DYSFUNCTION; METABOLIC DYSFUNCTION; CONTRACTILE FUNCTION; INDUCED CACHEXIA;

D O I：

10.1113/JP276746

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Cardiovascular diseases and cancer remain the leading cause of death worldwide. Despite the fact that these two conditions have long been considered as distinct clinical entities, recent epidemiological and experimental studies suggest that they should be contemplated and treated as co-morbidities. Heart failure represents nowadays a well-established complication of cancer, primarily as a consequence of the aggressive use of cardiotoxic anti-cancer treatments. On the other hand, the provocative idea that heart failure can prime carcinogenesis has started to emerge, though the molecular basis is still to be fully elucidated. This review summarizes the current knowledge on the mechanisms underlying the bidirectional communication between the failing heart and the cancer. We will discuss and/or speculate on the role of molecular mediators released by either the tumour or the heart that can potentially link heart failure and cancer.

引用

页码：3015 / 3027

页数：13

共 100 条

[21] Cancer Causes Cardiac Atrophy and Autophagy in a Sexually Dimorphic Manner [J].