Role for Mitochondria in ndothelial Function and Cardiovascular Diseases


Austin J Clin Cardiolog. 2014;1(2): 1018.

Role for Mitochondria in ndothelial Function and Cardiovascular Diseases

Yukio Shimasaki*

Global Medical Affairs Japan Department, Takeda Pharmaceutical Company Limited, Tokyo, Japan

*Corresponding author: Yukio Shimasaki, Global Medical Affairs Japan Department, Takeda Development Center Japan, Takeda Pharmaceutical Company Limited, 12-10, Nihonbashi 2-chome, Chuo-ku, Tokyo 103-8668, Japan

Received: March 10, 2014; Accepted: March 20, 2014; Published: March 24, 2014

A Wide Variety of Functions and Distinguishing Features of Mitochondria

Mitochondria are evolutionary remnants of aerobic bacteria that invaded protoeukaryotic cells a billion years ago. The ability to utilize oxygen drove the development and evolution of the cardiovascular system in multicellular organisms, and for this reason mitochondria are linked to the cardiovascular system from the earliest stages of evolution [1]. Their role in the cardiovascular system is an intense area of recent research contributing to the idea that mitochondrial dysfunction is essential to cardiovascular disease (CVD).

Mitochondria are considered to be the powerhouse of the cell being the primary generators of adenosine triphosphate (ATP) (Figure 1). Known mitochondrial functions extend beyond ATP production to include other cellular processes such as mitochondriaderived reactive oxygen species (ROS) signaling, Ca2+ signaling, apoptosis, heme synthesis [2], inflammation [3], and embryonic development [4]. Interestingly, mitochondria communicate with the endoplasmic reticulum (ER) because the ER is the largest consumer of mitochondrial ATP and mitochondria critically depend on ERderived Ca2+ [5,6]. The interorganelle communication is importantfor the vital exchange of lipids, Ca2+, and ATP.

In addition, mitochondria communicate a great deal with the nucleus to enable mitochondrial biogenesis, which occurs in response to various stimuli, from cold to fuel deprivation to exercise. The peroxisome proliferator–activated receptor–γcoactivator–1α (PGC– 1α) is a master regulator of mitochondrial biogenesis. It has been argued that PGC–1α–induced biogenesis protects against excessive mitochondrial ROS and oxidative stress by supplying undamaged mitochondria that produce less ROS [7].

Citation: Shimasaki Y. Role for Mitochondria in Endothelial Function and Cardiovascular Diseases. Austin J Clin Cardiolog. 2014;1(2): 1018. ISSN 2381-9111