Many articles focus on important research results of mitochondria!

In this paper, I have compiled many important research results, and jointly interpreted the new progress of scientists in the field of mitochondrial research, to share with you! Photo source: cc0 public domain [1] NAT Genet: uncover the mystery of mitochondrial genome or hope to help develop a variety of new cancer therapies doi: 10.1038/s41588-019-0557-x recently, an international journal Nature In the Research Report on genetics, scientists from Anderson Cancer Center of the University of Texas and other institutions have conducted in-depth research on the energy engineering of cells - mitochondria Because mitochondria play a key role in tumorigenesis, in-depth research on mitochondrial genome is essential to reveal the mechanism of tumorigenesis and develop new therapies Han Liang, researcher, said that this study laid the foundation for the transformation of mitochondrial biology research into clinical application Our analysis provided the most definite mutation blueprint of mitochondrial genome, and determined the status of multiple high mutations, such as truncated mutation It is suggested that activation of specific signaling pathways may have carcinogenic effects 【2】 Science: new research reveals that VDAC protein oligomer promotes mitochondrial DNA release and autoimmune response doi: 10.1126/science.aav4011 immune system uses its mitochondria to stimulate innate response and adaptive response to infection Active oxygen species (ROS), immunogenic mitochondrial DNA (mtDNA) and even the whole mitochondria are mobilized locally in a delicate balance, thus producing a hot spot of inflammatory effect When the normal restrictive feedback of these processes is destroyed, harmful autoimmune reactions often occur A common sign of abnormal immune system is the presence of anti mitochondrial antibody (AMA) in the blood For example, in systemic lupus erythematosus (SLE), AMA targeting multiple mitochondrial compartments can be found Some AMA targets proteins usually found in the outer mitochondrial membrane, while others target mtDNA One of the natural problems is how the immune system finds mtDNA released from mitochondria, given that mtDNA is normally located in the mitochondrial matrix To solve this problem, researchers from the national heart, lung and Blood Institute and other research institutions found in a new study that mtDNA released can cause lupus In short, when mitochondria are stressed in many ways, mtDNA breaks into fragments and binds to voltage dependent anion channels (VDAC) in the outer membrane of mitochondria This leads to the aggregation of VDAC monomers and the formation of a meta pore in the middle of them, through which mtDNA can escape Once entering the cytoplasm, a variety of non-specific sensing proteins, including the Toll receptor for single strand DNA and the gas-sting pathway for double strand DNA, will trigger mature type I interferon (IFN) response The relevant research results were recently published in the journal Science 【3】 Cell Rep: key elements of mitochondria regulate muscle function doi: 10.1016/j.celrep.2019.09.063 strenuous activities (such as marathon) will make our muscles become tired, sore or even damaged As time goes on, our muscle fibers will self repair through complex cellular processes Recently, a new study by the University of Thomas Jefferson's mitocare center, in collaboration with the National Center for genetic medicine of the child health system in Washington, D.C., has determined that the protein micu1 in mitochondria is the "power source" of all cells, and how it plays a key role in maintaining muscle size and function and repairing damaged muscle fibers These findings point to the potential role of micu1 in neuromuscular diseases, which is published in the recent journal Cell reports The contraction and relaxation of our muscles depend on the balance of calcium ions in each muscle fiber Some of these calcium is absorbed by mitochondria to promote metabolism and generate energy, while protein micu1 acts as the main regulator of calcium uptake in mitochondria Controlling calcium transport through micu1 helps coordinate the function of muscle fibers and their internal mitochondria, the researchers said The interruption of this connection will prevent the normal communication between mitochondria and muscles, thus making muscles more vulnerable to damage and unable to exert too much pressure 【4】 Mol Cell: how do cells protect themselves from mitochondrial defects? doi：10.1016/j.molcel.2019.09.026 Cells need mitochondria to use the energy stored in food Most of the proteins needed by mitochondria to maintain their functions are encoded in the nucleus When these proteins are synthesized in the cytoplasm, they are transported to the mitochondria Special signal sequences can promote the protein to enter the mitochondria Once the protein arrives in the mitochondria, the signal sequences will be removed The former researchers don't know the importance of removing the signal sequence, and they don't know why mistakes in this process can cause a series of diseases, such as heart or brain diseases Recently, an international magazine published in molecular In the Research Report on cell, scientists from the University of Freiburg and other institutions in Germany found that if there is an error in the process of signal sequence removal, it will lead to the accumulation of protein, so that it will continue to accumulate in mitochondria The accumulation of protein in mitochondria will promote the mitochondria to stop working However, all cells need the activity of mitochondria to maintain their survival 【5】 Nature: it is revealed that mitochondrial quality control defects can lead to heart disease doi: 10.1038/s41586-019-1667-4 mutations in a gene encoding adenine nucleotide transporter (ANT) can lead to many diseases, such as heart disease and ophthalmoplegia, but the underlying mechanism of how these mutations cause the disease is not clear Now, in a new study, researchers from the Perelman School of medicine at the University of Pennsylvania in the United States have revealed an amazing new function of ant: ant is critical to the quality control process of a type of mitochondrial autophagy, which helps ensure the integrity of the mitochondrial network by removing damaged mitochondria, and has found that it leads to such quality control The ant mutation with defects in the control system will eventually lead to heart disease, and relevant research results have been published in the journal Nature recently Ant is a well-known protein that helps mitochondria produce the chemical energy needed to drive the normal functioning of cells in the body, namely adenosine triphosphate (ATP) Although mutations in the ant gene are known to cause diseases, including cardiomyopathy, which makes it more difficult for the heart to pump blood to other parts of the body, studies have shown that these mutations do not affect the ability of ant to produce chemical energy, which raises questions about how people will get sick Photo source: cc0 public domain [6] NAT metal: the latest research challenges scientists' understanding of premature aging Mitochondrial DNA dysfunction may accelerate the aging process Doi: 10.1038/s42255-019-0120-1 recently, an international journal Nature In the Research Report on metabolism, scientists from the University of eastern Finland found that the disorder of mitochondrial DNA function may accelerate the aging process of the body in a different way than previously thought; the acceleration of aging may be the result of abnormal nucleotide level in cells and maintenance of damaged nuclear DNA Mitochondrion is a small organelle in cells, which has its own DNA mitochondrial DNA (mtDNA) For nearly half a century, mitochondrial DNA mutation and oxidative stress have been considered as the main factors leading to aging This is the hypothesis put forward in the theory of aging of mitochondria published in the 1970s This theory has been developed in mice with mtDNA mutation After testing, there is an inactive DNA modification mechanism in these mice These mice can accumulate mtDNA mutations and show the phenomenon of accelerated aging, which makes scientists believe that mtDNA mutations can lead to the occurrence of aging However, although several research groups have conducted serious research, no one can prove that the mutant mice will show the performance of oxidative stress rise 。 【7】 Ebiomedicine: mitochondrial regulatory factor or a new target for cancer treatment doi: 10.1016/j.ebiom.2019.09.017 recently, researchers from the Wistar Institute found the role of mitochondrial fission factor (MFF) in the control of cancer cell survival, indicating that the protein may represent a promising therapeutic target They also found that MFF expression was regulated by Myc The results are published online in the Journal ebiomedicine Mitochondria are organelles that provide energy to our cells They also control a variety of cell death mechanisms and play a complex role in cancer In addition, mitochondrial dynamics can coordinate the size, shape and location of mitochondria in cells, and then affect the progress of tumor, but until now, its mechanism has not been fully elucidated Reprogramming of mitochondrial function is crucial for cancer development and metastasis, the researchers say Our findings reveal new participants and new pathways in this process, opening up specific therapeutic opportunities for the selective elimination of tumor cells in patients " 【8】 Nature: an ATP sensitive potassium channel was identified in mitochondria Doi: 10.1038/s41586-019-1498-3 mitochondria are special organelles because they have their own DNA, which is called mitochondrial DNA (mtDNA) Unlike larger collections of DNA (genomes) that exist in the nucleus, mtDNA is transmitted only through the mother's egg cells MtDNA is also more likely to produce random changes or mutations in its DNA code than nuclear DNA These changes or mutations increase with the growth of human age However, this situation may also occur during the development of germ cells, leading to genetic diseases The incidence rate of these genetic diseases is about 1/4300 among American children Mitochondria are the energy factories of our cells Every day, the human body needs to produce ATP to provide energy for all cell activities Nerve impulses, muscle contractions, DNA replication and protein synthesis are just some examples of crucial processes that depend on the supply of ATP Mitochondria provide chemical energy for endogenous reactions in the form of ATP, and their activities must meet the energy needs of cells, but the mechanism of correlating this organelle performance with ATP level is poorly understood In a new study, researchers from the University of Padova in Italy confirmed that a protein complex in mitochondria mediates ATP dependent potassium current, which is called mitokatp, and the relevant research results were recently published in the journal Nature 【9】 Nature: mitochondrion fission requires protein drp1, but does not need dynamic protein doi: 10.1038/s41586-019-1296-y mitochondrion fission (sometimes translated as mitochondrion Division) is necessary to maintain the mitochondrial network, and depends on a GTP enzyme called dynamic related protein 1 (drp1, also known as dnm1l) Drp1 forms a spiral oligomer, which envelops the outer membrane of mitochondria and divides them Recently, it has been proposed that drp1 is not enough for mitochondrion fission, and the other is called dynamic-2 (dnm2, also known as Dyn2)