Sarcoplasmic reticulum–mitochondria communication

I think that the mitochondria is the best organelle in the cell, obviously, they're in the cell, his diameter is 0,5 - 1 μm and his length oscillates in 7 μm. The way that all the organelles depends of the mitochondria is interesting, because the mitochondria is responsible for generating energy.

Mitochondrial energy generation is of utmost importance in cells subject to high energy demand, as is the case for continuously contracting cardiomyocytes. Several studies have shown that mitochondrial disorders, with concomitant diminished mitochondrial function, are detrimental to heart performance, leading to cardiac hypertrophy and ultimately to heart failure. Moreover, vascular physiology is also dependent on mitochondrial function, because both growth and proliferation of vascular smooth muscle cells (VSMCs) are dependent on mitochondrial energetics. Impaired mitochondrial function has been associated with excessive VSMC proliferation, a hallmark of augmented arterial resistance, which leads to pathologies such as atherosclerosis and pulmonary artery hypertension. Taken together, this evidence highlights the importance of mitochondrial metabolism in cardiovascular physiology and disease.

Mitochondria, as well as other intracellular organelles, are highly dynamic structures that undergo constant changes in their mass, morphology, localization, and composition according to cellular requirements. Moreover, studies from different laboratories have shown physical and functional communication between mitochondria and other organelles, such as the plasma membrane, nucleus, and endoplasmic reticulum (ER). ER–mitochondria coupling was the first type of organelle interaction described, and was recognized early on as being required for lipid exchange and calcium ion (Ca²⁺) transfer. At ER–mitochondria contact points, Ca²⁺ is directly transferred to mitochondria from ER stores, and, when in the mitochondrial matrix, stimulates Krebs cycle activity and ATP synthesis. In muscle cells, where the ER is termed sarcoplasmic reticulum (SR), SR–mitochondria coupling is a critical regulator of cell metabolism.

In addition to the role in bioenergetics, Ca²⁺ release from the SR is crucial for VSMC and cardiomyocyte function, as both arterial and cardiac contraction are regulated by transient changes in cytosolic Ca²⁺ concentrations. Mitochondrial Ca²⁺ uptake is important for the modulation of muscle contraction, because mitochondria act as local Ca²⁺ buffers that participate in the shaping of Ca²⁺ signals. Disturbances in this Ca²⁺ buffering activity lead to abnormal increments in cytosolic Ca²⁺, which might activate different signalling pathways, including calcineurin and calcium/calmodulin-dependent protein kinase type II, both of which are associated with cardiac hypertrophy and HF. Interactions between the SR and mitochondria, as well as individual organelle morphology, are major determinants of efficient Ca²⁺ buffering and thus have an important role in both cardiomyocyte and VSMC physiology and dysfunction.

Some functions of mitochondria

The illnesses of mitochondria is related to mitochondrial dysfunction, mitochondrial diseases are sometimes (about 15% of the time) caused by mutations in the mitochondrial DNA that affect mitochondrial function. Other mitochondrial diseases are caused by mutations in genes of the nuclear DNA, whose gene products are imported into the mitochondria (mitochondrial proteins) as well as acquired mitochondrial conditions. Mitochondrial diseases take on unique characteristics both because of the way the diseases are often inherited and because mitochondria are so critical to cell function. The subclass of these diseases that have neuromuscular disease symptoms are often called a mitochondrial myopathy.

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. So the recommendation is don't take medications without knowing their side effects.

Confocal microscopy of mitochondria