Researchers have reviewed the role of mitochondria in cardiac diseases, highlighting different aspects of these multifaceted organelles and pointing out key processes, that, if deregulated, can lead to heart disease.
Heart muscle cells – or cardiomyocytes – rely heavily on mitochondria for their energy needs. Different mitochondrial processes that can be deregulated in someone with heart disease include regulation of the free radicals (which produce oxidative tissue damage), energy supply, and protein death.
According to the review, when it comes to mitochondria contributing to or sensing damage in the heart cells, attention should be paid to three parameters:
- A detoxification network within the mitochondria;
- The amount and function of specific proteins, including those called chaperones, that safeguard mitochondrial integrity;
- The control of mitochondrial shape and number (through mitochondrial union and clearance).
Mitochondria Processes: What can go wrong
There is a growing body of scientific literature implicating the increased generation and accumulation of cellular toxic waste – both of which can be traced back to mitochondrial malfunction – with cardiac failure and ischemic attacks (neurological dysfunction caused by loss of blood flow).
Additionally, changes in the expression of specific proteins, whether encoded in the mitochondria or not, can also affect how these organelles are able to cope during stress related to heart problems.
To complicate things further, there is a disruption in the cellular response that deals with defective proteins, which has also been associated with cardiac problems.
Finally, maintaining mitochondrial size, shape, number, and location through mitochondrial merger and separation and mitophagy (the selective degradation of mitochondria) is just as important when it comes to healthy heart cells. When these processes are disrupted, cardiovascular diseases are far more likely to occur due to the accumulation of problematic mitochondria.
“The importance of functional mitochondrial to the heart has been highlighted by the fact that situations that lead to mitochondrial dysfunction are often associated with cardiac diseases,” the authors wrote in the report.
“Many of these diseases manifest later in life, where mitochondria seems to be less functional. Therefore, different levels of mechanisms of surveillance and quality control capable of detecting and fixing defects that affect mitochondrial performance are critical for the maintenance of long-lived cells with high energy demand such as cardiomyocytes.”
“However, future research focusing on the critical molecular events involved in mitochondrial quality control is needed to develop better pharmacological interventions,” the authors wrote in their review, emphasizing the need for additional experiments and clinical trials that analyze key parameters of mitochondrial performance.