Tanaka Shota, Fujio Yasushi, Nakayama Hiroyuki
Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Front Physiol. 2018 Aug 7;9:1081. doi: 10.3389/fphys.2018.01081. eCollection 2018.
Cardiac hypertrophy is a major risk for the progression of heart failure; however, the underlying molecular mechanisms contributing to this process remain elusive. The caveolae microdomain plays pivotal roles in various cellular processes such as lipid homeostasis, signal transduction, and endocytosis, and also serves as a signaling platform. Although the caveolae microdomain has been postulated to have a major contribution to the development of cardiac pathologies, including cardiac hypertrophy, recent evidence has placed this role into question. Lack of direct evidence and appropriate methods for determining activation of caveolae-specific signaling has thus far limited the ability to obtain a definite answer to the question. In this review, we focus on the potential physiological and pathological roles of the multifunctional kinase Ca/calmodulin-dependent kinase II and voltage-dependent L-type calcium channel in the caveolae, toward gaining a better understanding of the contribution of caveolae-based signaling in cardiac hypertrophy.
心脏肥大是心力衰竭进展的主要风险因素；然而，导致这一过程的潜在分子机制仍不清楚。小窝微区在脂质稳态、信号转导和内吞作用等各种细胞过程中发挥着关键作用，并且还充当信号平台。尽管小窝微区被认为对包括心脏肥大在内的心脏病理发展有重要贡献，但最近的证据对此作用提出了质疑。迄今为止，缺乏确定小窝特异性信号激活的直接证据和适当方法，限制了我们对这个问题得出明确答案的能力。在这篇综述中，我们聚焦于多功能激酶钙/钙调蛋白依赖性激酶II和电压依赖性L型钙通道在小窝中的潜在生理和病理作用，以便更好地理解基于小窝的信号传导在心脏肥大中的作用。
