An interesting paper was published in the week before Christmas. Mitochondrial quality control: the real dawn of intervertebral disc degeneration?
The summary states: Intervertebral disc degeneration is the most common disease in chronic musculoskeletal diseases and the main cause of low back pain, which seriously endangers social health level and increases people’s economic burden. Disc degeneration is characterized by NP cell apoptosis, extracellular matrix degradation and disc structure changes. It progresses with age and under the influence of mechanical overload, oxidative stress and genetics. Mitochondria are not only the energy factories of cells, but also participate in a variety of cellular functions such as calcium homeostasis, regulation of cell proliferation, and control of apoptosis. The mitochondrial quality control system involves many mechanisms such as mitochondrial gene regulation, mitochondrial protein import, mitophagy, and mitochondrial dynamics. A large number of studies have confirmed that mitochondrial dysfunction is a key factor in the pathological mechanism of aging and intervertebral disc degeneration, and balancing mitochondrial quality control is extremely important for delaying and treating intervertebral disc degeneration. In this paper, we first demonstrate the molecular mechanism of mitochondrial quality control in detail by describing mitochondrial biogenesis and mitophagy. Then, we describe the ways in which mitochondrial dysfunction leads to disc degeneration, and review in detail the current research on targeting mitochondria for the treatment of disc degeneration, hoping to draw inspiration from the current research to provide innovative perspectives for the treatment of disc degeneration.
I like this paper because it goes into a lot of detail about improving the quality of mitochondria. I am not as enthused at their proposal of injecting exosomes. I take the view that if we wish to improve the quality of mitochondria the bad ones need to go. There is no sense fusing them as the bad mtDNA is not selected against. On the other hand when mitophagy occurs the worse mitochondria are preferentially removed.
However, what this paper is good at is looking at the links between mitochondria and the Extra Cellular Matrix (ECM). People have recognised the importance of the ECM and a view has been expressed that it cannot be repaired. However, I think the paper is right to identify efficient mitochondria as a route towards a better ECM. The paper does not look at the links between the Mitochodrial Membrane Potential and the nature of proteins produced (either alternative splices or not at all). However, it is a useful review as to maintenance of Mitochondria.
The summary states: Intervertebral disc degeneration is the most common disease in chronic musculoskeletal diseases and the main cause of low back pain, which seriously endangers social health level and increases people’s economic burden. Disc degeneration is characterized by NP cell apoptosis, extracellular matrix degradation and disc structure changes. It progresses with age and under the influence of mechanical overload, oxidative stress and genetics. Mitochondria are not only the energy factories of cells, but also participate in a variety of cellular functions such as calcium homeostasis, regulation of cell proliferation, and control of apoptosis. The mitochondrial quality control system involves many mechanisms such as mitochondrial gene regulation, mitochondrial protein import, mitophagy, and mitochondrial dynamics. A large number of studies have confirmed that mitochondrial dysfunction is a key factor in the pathological mechanism of aging and intervertebral disc degeneration, and balancing mitochondrial quality control is extremely important for delaying and treating intervertebral disc degeneration. In this paper, we first demonstrate the molecular mechanism of mitochondrial quality control in detail by describing mitochondrial biogenesis and mitophagy. Then, we describe the ways in which mitochondrial dysfunction leads to disc degeneration, and review in detail the current research on targeting mitochondria for the treatment of disc degeneration, hoping to draw inspiration from the current research to provide innovative perspectives for the treatment of disc degeneration.
I like this paper because it goes into a lot of detail about improving the quality of mitochondria. I am not as enthused at their proposal of injecting exosomes. I take the view that if we wish to improve the quality of mitochondria the bad ones need to go. There is no sense fusing them as the bad mtDNA is not selected against. On the other hand when mitophagy occurs the worse mitochondria are preferentially removed.
However, what this paper is good at is looking at the links between mitochondria and the Extra Cellular Matrix (ECM). People have recognised the importance of the ECM and a view has been expressed that it cannot be repaired. However, I think the paper is right to identify efficient mitochondria as a route towards a better ECM. The paper does not look at the links between the Mitochodrial Membrane Potential and the nature of proteins produced (either alternative splices or not at all). However, it is a useful review as to maintenance of Mitochondria.
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