Takotsubo综合征的最新发病机制:"急性冠状动脉综合征的终结

IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Journal of molecular and cellular cardiology Pub Date : 2024-04-18 DOI:10.1016/j.yjmcc.2024.04.009
Filippo Crea , Giulia Iannaccone , Giulia La Vecchia , Rocco A. Montone
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引用次数: 0

摘要

高猝死综合征(TTS)是一种急性可逆性心肌功能障碍,通常在发病前有身体或情绪上的应激事件作为诱因。尽管最近在理解导致 TTS 的机制方面取得了进展,但对其病理生理学的理解还远远不够。本文旨在回顾 TTS 复杂的病理生理学以及该临床症状可能存在的不同机制,重点关注冠状动脉微血管功能障碍的作用以及该领域尚存的知识空白。
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An update on the mechanisms of Takotsubo syndrome: “At the end an acute coronary syndrome”

Takotsubo syndrome (TTS) is an acute reversible form of myocardial dysfunction, often preceded by a physical or emotional stressful event, that acts as a trigger. Despite, recent advances in the comprehension of the mechanisms leading to TTS, its pathophysiology is far from being completely understood. However, several studies seem to suggest that an acute coronary microvascular dysfunction may represent a crucial pathogenic mechanism involved in TTS occurrence.

In this article, we aim to review the complex pathophysiology of TTS and the possible different mechanisms underlying this clinical condition, focusing on the role of coronary microvascular dysfunction and the remaining knowledge's gaps in the field.

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来源期刊
CiteScore
10.70
自引率
0.00%
发文量
171
审稿时长
42 days
期刊介绍: The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.
期刊最新文献
Editorial Board PERM1 regulates mitochondrial energetics through O-GlcNAcylation in the heart Corrigendum to "PGE2 protects against heart failure through inhibiting TGF-β1 synthesis in cardiomyocytes and crosstalk between TGF-β1 and GRK2" [Journal of Molecular and Cellular Cardiology. 172(2022) 63-77]. Retraction notice to “The novel antibody fusion protein rhNRG1-HER3i promotes heart regeneration by enhancing NRG1-ERBB4 signaling pathway” [Journal of Molecular and Cellular Cardiology 187 (2023) 26–37] Exercise training attenuates cardiac dysfunction induced by excessive sympathetic activation through an AMPK-KLF4-FMO2 axis
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