Interactive Roles of CaMKII/Ryanodine Receptor Signaling and Inflammation in Lung Diseases

Wang, Lan; Ginnan, Roman; Wang, Yong-Xiao; Zheng, Yun‐Min

doi:10.1007/978-3-030-63046-1_16

Cited by 1 publication

(1 citation statement)

References 87 publications

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“…CaMKII is a vital kinase in the modulation of the activity of multiple Ca 2+ ‐handling proteins, including RYR2 (Erickson et al, 2011; Wehrens et al, 2004). The production of ROS has been proposed to be an essential process for the elevation of CaMKII activity, manifesting as phosphorylation and oxidation of CaMKII (Erickson et al, 2011; Wang et al, 2021). A very recent study found that ROS‐CaMKII–RYR2 pathway contributed to disordered calcium handling and damaged cardiac muscle contraction in Barth syndrome (Liu et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Impact and potential mechanism of effects of chronic moderate alcohol consumption on cardiac function in aldehyde dehydrogenase 2 gene heterozygous mice

Chen

Cheng

et al. 2022

Alcoholism Clin & Exp Res

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Background Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is a key enzyme in alcohol metabolism. The ALDH2*2 mutations are found in approximately 45% of East Asians, with 40% being heterozygous (HE) ALDH2*1/*2 and 5% homozygous (HO) ALDH2*2/*2. Studies have shown that HO mice lack cardioprotective effects induced by moderate alcohol consumption. However, the impact of moderate alcohol consumption on cardiac function in HE mice is unknown. Methods In this study, HO, HE, and wild‐type (WT) mice were subjected to a 6‐week moderate alcohol drinking protocol, following which myocardial tissue and cardiomyocytes of the mice were extracted. Results We found that moderate alcohol exposure did not increase mortality, myocardial fibrosis, apoptosis, or inflammation in HE mice, which differs from the effects observed in HO mice. After exposure to the 6‐week alcohol drinking protocol, there was impaired cardiac function, cardiomyocyte contractility, and intracellular Ca2+ homeostasis and mitochondrial function in both HE and HO mice as compared to WT mice. Moreover, these animals showed overt oxidative stress production and increased levels of the activated forms of calmodulin‐dependent protein kinase II (CaMKII) and ryanodine receptor type 2 (RYR2) phosphorylation protein. Conclusion We found that moderate alcohol exposure impaired cardiac function in HE mice, possibly by increasing reactive oxygen species (ROS)/CaMKII/RYR2‐mediated Ca2+ handling abnormalities. Hence, we advocate that people with ALDH2*1/*2 genotypes rigorously avoid alcohol consumption to prevent potential cardiovascular harm induced by moderate alcohol consumption.

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