Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).
Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).
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DOI：
10.1002/ejhf.2029
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发表时间：
2020-12
影响因子：
18.2
通讯作者：
Backs J
中科院分区：
文献类型：
--
作者：
de Boer RA;Hulot JS;Tocchetti CG;Aboumsallem JP;Ameri P;Anker SD;Bauersachs J;Bertero E;Coats AJS;Čelutkienė J;Chioncel O;Dodion P;Eschenhagen T;Farmakis D;Bayes-Genis A;Jäger D;Jankowska EA;Kitsis RN;Konety SH;Larkin J;Lehmann L;Lenihan DJ;Maack C;Moslehi JJ;Müller OJ;Nowak-Sliwinska P;Piepoli MF;Ponikowski P;Pudil R;Rainer PP;Ruschitzka F;Sawyer D;Seferovic PM;Suter T;Thum T;van der Meer P;Van Laake LW;von Haehling S;Heymans S;Lyon AR;Backs J
癌症和心力衰竭（HF）的共同发生代表了一个显著的临床缺陷，因为每种疾病都会干扰另一种疾病的治疗。除了共同的风险因素外，越来越多的实验和临床证据揭示了两种病理基础的生物学方面的许多共同点。炎症是这两种疾病的共同标志，因为它有助于HF和癌症的发生和发展。在压力下，恶性细胞和心脏细胞会改变它们的代谢偏好以生存，这使得这些代谢紊乱成为开发交叉策略和治疗方法以对抗这两种疾病的重要基础。此外，遗传易感性和克隆造血是这两种情况的共同驱动因素，它们在个性化医疗的背景下具有很大的临床意义。此外，改变的血管生成是心脏衰竭和肿瘤的共同标志，并且代表了在这两种疾病中靶向的有希望的底物。心脏细胞和恶性细胞与其周围的环境相互作用，称为基质。这种相互作用介导了两种病理的进展，了解每种基质成分的结构和功能可能为创新的治疗策略和改善患者的预后铺平道路。心脏病学家和肿瘤学家之间的跨学科合作对于建立统一的指南至关重要。为此，需要模拟人类情况的临床前模型，其中两种病理共存，以了解癌症和HF之间双向关系的所有方面。最后，充分的临床研究，包括所有年龄段的患者，男性和女性，以及对癌症和心血管终点的适当裁定，对于同时准确研究这两种病理是至关重要的。我们描述了癌症和心力衰竭（HF）的共同发生，其潜在的共同风险因素及其病理生理机制。我们提倡心脏病学家和肿瘤学家之间的密切互动，以实现统一的假设和合作的临床前和临床研究。
The co‐occurrence of cancer and heart failure (HF) represents a significant clinical drawback as each disease interferes with the treatment of the other. In addition to shared risk factors, a growing body of experimental and clinical evidence reveals numerous commonalities in the biology underlying both pathologies. Inflammation emerges as a common hallmark for both diseases as it contributes to the initiation and progression of both HF and cancer. Under stress, malignant and cardiac cells change their metabolic preferences to survive, which makes these metabolic derangements a great basis to develop intersection strategies and therapies to combat both diseases. Furthermore, genetic predisposition and clonal haematopoiesis are common drivers for both conditions and they hold great clinical relevance in the context of personalized medicine. Additionally, altered angiogenesis is a common hallmark for failing hearts and tumours and represents a promising substrate to target in both diseases. Cardiac cells and malignant cells interact with their surrounding environment called stroma. This interaction mediates the progression of the two pathologies and understanding the structure and function of each stromal component may pave the way for innovative therapeutic strategies and improved outcomes in patients. The interdisciplinary collaboration between cardiologists and oncologists is essential to establish unified guidelines. To this aim, pre‐clinical models that mimic the human situation, where both pathologies coexist, are needed to understand all the aspects of the bidirectional relationship between cancer and HF. Finally, adequately powered clinical studies, including patients from all ages, and men and women, with proper adjudication of both cancer and cardiovascular endpoints, are essential to accurately study these two pathologies at the same time. We describe the co‐occurrence of cancer and heart failure (HF), their potential shared risk factors, and their pathophysiological mechanisms. We advocate intense interaction between cardiologists and oncologists to achieve unifying hypotheses and collaborative pre‐clinical and clinical studies.
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DOI：
10.1002/jcsm.12126
发表时间：
2016-06
期刊：
Journal of cachexia, sarcopenia and muscle
影响因子：
--
作者：
Stewart Coats AJ;Ho GF;Prabhash K;von Haehling S;Tilson J;Brown R;Beadle J;Anker SD;for and on behalf of the ACT‐ONE study group
通讯作者：
for and on behalf of the ACT‐ONE study group
影响因子：
82.9
作者：
Koelwyn GJ;Newman AAC;Afonso MS;van Solingen C;Corr EM;Brown EJ;Albers KB;Yamaguchi N;Narke D;Schlegel M;Sharma M;Shanley LC;Barrett TJ;Rahman K;Mezzano V;Fisher EA;Park DS;Newman JD;Quail DF;Nelson ER;Caan BJ;Jones LW;Moore KJ
通讯作者：
Moore KJ
影响因子：
9.8
作者：
Acuna-Hidalgo, Rocio;Sengul, Hilal;Hoischen, Alexander
通讯作者：
Hoischen, Alexander
影响因子：
--
作者：
ALLARD, MF;SCHONEKESS, BO;LOPASCHUK, GD
通讯作者：
LOPASCHUK, GD
分子机制和血管生成的临床应用。
影响因子：
64.8
作者：
Carmeliet, Peter;Jain, Rakesh K.
通讯作者：
Jain, Rakesh K.