I agree that faulty mitochondria will break homeostasis and from this point on, the problem is unsolvable.
But homeostasis will break because:
1. Plain vanilla energy deficit. Not enough energy. Babies die within the first days after birth. or 2. Inefficient - but normal - energy production. This will produce an excess of free radicals, "emitting" all kinds of weird signals to the rest of the cell/tissue/body. Most of mitochondrial diseases and diseases that cause a secondary mitochondrial dysfunction fall in this category. "The threshold effect" - mutant mitochondria outnumber healthy mitochondria as you grow older - will eventually take you to point 1.
Given this, repairing the mitochondria will bring homeostasis back. Currently, there are 3 lines of thought: 1. Repair the faulty mitochondria 2. Allotopic expression (literally, make backup copies of mitochondria DNA in the nuclear DNA and let them "express" from here instead of from mtDNA) 3. Kill faulty mitochondria. Given that mitochondria go through a fusion/fission cycles every few days, killing faulty mitochondria will restore a healthy mitochondria population in a very short period. The underlying genetic defect is still there, but it causes no harm at all.
I am for 3.; much simpler both technically and legally. The latest in this regards is http://onlinelibrary.wiley.com/doi/10.1002/emmm.201303672/ab...
Thanks for your concert. I didn´t want to be tragic in my original post. My life depends on my mitochondria, but I am doing relatively well considering my disease.
For the curious, I have CPEO + myopathy, common mtDNA deletion, 35% mutation load.
I'm a Ph.D. candidate in systems biology.
Then, we have anti-aging. Big business here. Mitochondria is key.
Then, we have diseases with secondary mitochondrial dysfunction. Again, big business (Alzheimer, Type 2 diabetes, statin-induced myopathy, etc)
There are many diferrent figures as "mitochondrial disease" is a broad term, but check these out: http://ije.oxfordjournals.org/content/41/1/177.long http://www.ncbi.nlm.nih.gov/pubmed/18674747?dopt=Abstract