Editing Mitochondrion (section)

===Cellular proliferation regulation===
The relationship between cellular proliferation and mitochondria has been investigated. Tumor cells require ample ATP to synthesize bioactive compounds such as [[lipid]]s, [[protein]]s, and [[nucleotide]]s for rapid proliferation.<ref name="Weinberg-2009">{{cite journal | vauthors = Weinberg F, Chandel NS | title = Mitochondrial metabolism and cancer | journal = Annals of the New York Academy of Sciences | volume = 1177 | issue = 1 | pages = 66–73 | date = October 2009 | pmid = 19845608 | doi = 10.1111/j.1749-6632.2009.05039.x | bibcode = 2009NYASA1177...66W }}</ref> The majority of ATP in tumor cells is generated via the [[oxidative phosphorylation]] pathway (OxPhos).<ref name="Moreno-Sánchez-2007">{{cite journal | vauthors = Moreno-Sánchez R, Rodríguez-Enríquez S, Marín-Hernández A, Saavedra E | title = Energy metabolism in tumor cells | journal = The FEBS Journal | volume = 274 | issue = 6 | pages = 1393–1418 | date = March 2007 | pmid = 17302740 | doi = 10.1111/j.1742-4658.2007.05686.x }}</ref> Interference with OxPhos cause [[cell cycle]] arrest suggesting that mitochondria play a role in cell proliferation.<ref name="Moreno-Sánchez-2007"/> Mitochondrial ATP production is also vital for [[cell division]] and differentiation in infection<ref>{{cite journal | vauthors = Mistry JJ, Marlein CR, Moore JA, Hellmich C, Wojtowicz EE, Smith JG, Macaulay I, Sun Y, Morfakis A, Patterson A, Horton RH, Divekar D, Morris CJ, Haestier A, Di Palma F, Beraza N, Bowles KM, Rushworth SA | title = ROS-mediated PI3K activation drives mitochondrial transfer from stromal cells to hematopoietic stem cells in response to infection | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 116 | issue = 49 | pages = 24610–24619 | date = December 2019 | pmid = 31727843 | pmc = 6900710 | doi = 10.1073/pnas.1913278116 | doi-access = free | bibcode = 2019PNAS..11624610M }}</ref> in addition to basic functions in the cell including the regulation of cell volume, solute [[concentration]], and cellular architecture.<ref name="Pedersen-1994">{{cite journal | vauthors = Pedersen PL | title = ATP synthase. The machine that makes ATP | journal = Current Biology | volume = 4 | issue = 12 | pages = 1138–1141 | date = December 1994 | pmid = 7704582 | doi = 10.1016/S0960-9822(00)00257-8 | bibcode = 1994CBio....4.1138P }}</ref><ref name="Pattappa-2011">{{cite journal | vauthors = Pattappa G, Heywood HK, de Bruijn JD, Lee DA | title = The metabolism of human mesenchymal stem cells during proliferation and differentiation | journal = Journal of Cellular Physiology | volume = 226 | issue = 10 | pages = 2562–2570 | date = October 2011 | pmid = 21792913 | doi = 10.1002/jcp.22605 }}</ref><ref name="Agarwal-2011">{{cite journal | vauthors = Agarwal B | title = A role for anions in ATP synthesis and its molecular mechanistic interpretation | journal = Journal of Bioenergetics and Biomembranes | volume = 43 | issue = 3 | pages = 299–310 | date = June 2011 | pmid = 21647635 | doi = 10.1007/s10863-011-9358-3 }}</ref> ATP levels differ at various stages of the cell cycle suggesting that there is a relationship between the abundance of ATP and the cell's ability to enter a new cell cycle.<ref name="Sweet-1999">{{cite journal | vauthors = Sweet S, Singh G | title = Changes in mitochondrial mass, membrane potential, and cellular adenosine triphosphate content during the cell cycle of human leukemic (HL-60) cells | journal = Journal of Cellular Physiology | volume = 180 | issue = 1 | pages = 91–96 | date = July 1999 | pmid = 10362021 | doi = 10.1002/(SICI)1097-4652(199907)180:1<91::AID-JCP10>3.0.CO;2-6 }}</ref> ATP's role in the basic functions of the cell make the [[cell cycle]] sensitive to changes in the availability of mitochondrial derived ATP.<ref name="Sweet-1999"/> The variation in ATP levels at different stages of the cell cycle support the hypothesis that mitochondria play an important role in cell cycle regulation.<ref name="Sweet-1999"/> Although the specific mechanisms between mitochondria and the cell cycle regulation is not well understood, studies have shown that low energy cell cycle checkpoints monitor the energy capability before committing to another round of cell division.<ref name="McBride-2006"/>