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心脏舒张期钙的控制：基本机制与功能意义。

The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.

机构信息

From the Unit of Cardiac Physiology, Division of Cardiovascular Sciences, University of Manchester, United Kingdom.

出版信息

Circ Res. 2020 Jan 31;126(3):395-412. doi: 10.1161/CIRCRESAHA.119.315891. Epub 2020 Jan 30.

DOI:10.1161/CIRCRESAHA.119.315891
PMID:31999537
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7004450/
Abstract

Normal cardiac function requires that intracellular Ca concentration be reduced to low levels in diastole so that the ventricle can relax and refill with blood. Heart failure is often associated with impaired cardiac relaxation. Little, however, is known about how diastolic intracellular Ca concentration is regulated. This article first discusses the reasons for this ignorance before reviewing the basic mechanisms that control diastolic intracellular Ca concentration. It then considers how the control of systolic and diastolic intracellular Ca concentration is intimately connected. Finally, it discusses the changes that occur in heart failure and how these may result in heart failure with preserved versus reduced ejection fraction.

摘要

正常的心脏功能要求细胞内 Ca 浓度在舒张期降低到低水平，以使心室能够放松并重新充满血液。心力衰竭通常与心脏舒张功能障碍有关。然而，关于如何调节舒张期细胞内 Ca 浓度知之甚少。本文首先讨论了造成这种无知的原因，然后回顾了控制舒张期细胞内 Ca 浓度的基本机制。接着考虑了收缩期和舒张期细胞内 Ca 浓度的控制是如何紧密相连的。最后，讨论了心力衰竭时发生的变化，以及这些变化如何导致射血分数保留型心力衰竭和射血分数降低型心力衰竭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/ae91f1667b18/res-126-395-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/19b841e808ea/res-126-395-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/f0df6d2dd392/res-126-395-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/81719d865d0e/res-126-395-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/ae91f1667b18/res-126-395-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/19b841e808ea/res-126-395-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/b67cff4182a7/res-126-395-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/f0df6d2dd392/res-126-395-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/81719d865d0e/res-126-395-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de6d/7004450/ae91f1667b18/res-126-395-g005.jpg

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The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.

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本文引用的文献

[1]
Long-term effects of Na /Ca exchanger inhibition with ORM-11035 improves cardiac function and remodelling without lowering blood pressure in a model of heart failure with preserved ejection fraction.

Eur J Heart Fail. 2019-11-24

[2]
HFpEF-Time to Explore the Role of Genetic Heterogeneity in Phenotypic Variability: New Mechanistic Insights Offer Promise for Personalized Therapies.

Circulation. 2019-11-12

[3]
Disturbed cardiac mitochondrial and cytosolic calcium handling in a metabolic risk-related rat model of heart failure with preserved ejection fraction.

Acta Physiol (Oxf). 2020-3

[4]
Disruption of Ca Homeostasis and Connexin 43 Hemichannel Function in the Right Ventricle Precedes Overt Arrhythmogenic Cardiomyopathy in Plakophilin-2-Deficient Mice.

Circulation. 2019-7-18

[5]
Heart Failure With Preserved Ejection Fraction In Perspective.

Circ Res. 2019-5-24

[6]
Calcium Buffering in the Heart in Health and Disease.

Circulation. 2019-5-14

[7]
Nitrosative stress drives heart failure with preserved ejection fraction.

Nature. 2019-4-10

[8]
Structural features of STIM and Orai underlying store-operated calcium entry.

Curr Opin Cell Biol. 2019-2-1

[9]
Potential Arrhythmogenic Role of TRPC Channels and Store-Operated Calcium Entry Mechanism in Mouse Ventricular Myocytes.

Front Physiol. 2018-12-13

[10]
Early calcium handling imbalance in pressure overload-induced heart failure with nearly normal left ventricular ejection fraction.

Biochim Biophys Acta Mol Basis Dis. 2018-8-4

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