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. 2013 Dec 18;1(3):109-21.
doi: 10.4103/2321-3868.123072. eCollection 2013.

Inflammation and cardiac dysfunction during sepsis, muscular dystrophy, and myocarditis

Ying Li  1 , Shuping Ge  2 , Yizhi Peng  3 , Xiongwen Chen  4
Affiliations

Inflammation and cardiac dysfunction during sepsis, muscular dystrophy, and myocarditis

Ying Li et al. Burns Trauma. .

Abstract

Inflammation plays an important role in cardiac dysfunction under different situations. Acute systemic inflammation occurring in patients with severe burns, trauma, and inflammatory diseases causes cardiac dysfunction, which is one of the leading causes of mortality in these patients. Acute sepsis decreases cardiac contractility and impairs myocardial compliance. Chronic inflammation such as that occurring in Duchenne muscular dystropshy and myocarditis may cause adverse cardiac remodeling including myocyte hypertrophy and death, fibrosis, and altered myocyte function. However, the underlying cellular and molecular mechanisms for inflammatory cardiomyopathy are still controversial probably due to multiple factors involved. Potential mechanisms include the change in circulating blood volume; a direct inhibition of myocyte contractility by cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β); abnormal nitric oxide and reactive oxygen species (ROS) signaling; mitochondrial dysfunction; abnormal excitation-contraction coupling; and reduced calcium sensitivity at the myofibrillar level and blunted β-adrenergic signaling. This review will summarize recent advances in diagnostic technology, mechanisms, and potential therapeutic strategies for inflammation-induced cardiac dysfunction.

Keywords: Burn; Duchenne muscular dystrophy; cardiac dysfunction; contractility; inflammation; sepsis.

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Figures

Figure 1:
Figure 1:
Scheme of cellular structures and molecules involved in excitation-contraction coupling in ventricular myocytes. The black stars indicate Ca2+ ions. Solid lines indicate Ca2+ influx into cytosol and dotted lines indicate Ca2+ extrusion pathways. The thickness of the line indicates the relative contribution of each pathway. LTCC = L-type Ca2+ channel, NCX = sodium-calcium exchanger, PLB = phospholamban, RyR = ryanodine receptor, SR = sarcoplasmic reticulum, SERCA = sarcoplasmic reticulum Ca2+ ATPase.
Figure 2:
Figure 2:
Mechanisms for cardiac dysfunction induced by inflammation.
See this image and copyright information in PMC

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