[1] McMillan RP, Stewart S, Budnick JA, Caswell CC. Quantitative variation in m.3243A> G mutation produce discrete changes in energy metabolism[J]. Sci Rep, 2019, 9:5752.
[2] Crimi M, Bordoni A, Menozzi G, Riva L, Fortunato F, Galbiati S, Del Bo R, Pozzoli U, Bresolin N, Comi GP. Skeletal muscle gene expression profiling in mitochondrial disorders[J]. FASEB J, 2005, 19:866-868.
[3] Mende S, Royer L, Herr A, Schmiedel J, Deschauer M, Klopstock T, Kostic VS, Schroeder M, Reichmann H, Storch A. Whole blood genome-wide expression profiling and network analysis suggest MELAS master regulators[J]. Neurol Res, 2011, 33:638-655.
[4] Pavlakis SG, Phillips PC, DiMauro S, De Vivo DC, Rowland LP. Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes:a distinctive clinical syndrome[J]. Ann Neurol, 1984, 16:481-488.
[5] Goto Y, Nonaka I, Horai S. A mutation in the tRNA (Leu) (UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies[J]. Nature, 1990, 348:651-653.
[6] Zhang J, Guo JH, Fang WH, Jun Q, Shi K. Clinical features of MELAS and its relation with A3243G gene point mutation[J]. Int J Clin Exp Pathol, 2015, 8:13411-13415.
[7] Adams JM, Cory S. Bcl-2-regulated apoptosis mechanism and therapeutic potential[J]. Curr Opin Immunol, 2007, 19:488-496.
[8] Ouyang YB, Giffard RG. MicroRNAs affect Bcl-2 family proteins in the setting of cerebral ischemia[J]. Neurochem Int, 2014, 77:2-8.
[9] Kuwana T, Bouchier-Hayes L, Chipuk JE, Bonzon C, Sullivan B, Green DR, Newmeyer DD. BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly[J]. Mol Cell, 2005, 17:525-535.
[10] Zhang LS, Li JJ, Wu CY. Research progress on the mechanism of cerebral ischemia injury and related signaling pathways[J]. Shen Jing Jie Pou Xue Za Zhi, 2014, 30:729-732.[张蔺珊, 李娟娟, 吴春云. 脑缺血的损伤机制及相关信号通路的研究进展[J]. 神经解剖学杂志, 2014, 30:729-732.]
[11] Zhuo B, Li Y, Li Z, Qin H, Sun Q, Zhang F, Shen Y, Shi Y, Wang R. PI3K/Akt signaling mediated hexokinase-2 expression inhibits cell apoptosis and promotes tumor growth in pediatric osteosarcoma[J]. Biochem Biophys Res Commun, 2015, 464:401-406.
[12] Zhou H, Zhang Y, Hu S, Shi C, Zhu P, Ma Q, Jin Q, Cao F, Tian F, Chen Y. Melatonin protects cardiac microvasculature against ischemia/reperfusion injury via suppression of mitochondrial fission-VDAC1-HK2-mPTP-mitophagy axis[J]. J Pineal Res, 2017, 63:12413.
[13] Miyamoto S, Murphy AN, Brown JH. Akt mediates mitochondrial protection in cardiomyocytes through phosphorylation of mitochondrial hexokinase-Ⅱ[J]. Cell Death Differ, 2008, 15:521-529.
[14] Zorov DB, Juhaszova M, Sollott SJ. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release[J]. Physiol Rev, 2014, 94:909-950.
[15] Ristow M, Schmeisser K. Mitohormesis:promoting health and lifespan by increased levels of reactive oxygen species (ROS)[J]. Dose Response, 2014, 12:288-341.
[16] Wei J, Zhang Y, Luo Y, Wang Z, Bi SL, Song D, Dai Y, Wang T, Qiu LX, Wen L, Yuan L, Yang JY. Aldose reductase regulates miR-200a-3p/141-3p to coordinate Keap1-Nrf2, TGFβ 1/2, and Zeb1/2 signaling in renal mesangial cells and the renal cortex of diabetic mice[J]. Free Radic Biol Med, 2014, 67:91-102.
[17] Giannoni E, Parri M, Chiarugi P. EMT and oxidative stress:a bidirectional interplay affecting tumor malignancy[J]. Antioxid Redox Signal, 2012, 16:1248-1263.
[18] Zhang JX, Liu Y, Zhang W, Zhou QB, Kong DQ, Liu R, Hai CX. Alteration of mitochondrial synthesis and function in epithelial-mesenchymal transition by TGF-β1[J]. Ai Bian·Ji Bian·Tu Bian, 2017, 29:411-417.[张佳欣, 刘颖, 张伟, 周庆彪, 孔德钦, 刘瑞,海春旭. TGF-β1诱导上皮间质转化过程中线粒体合成与功能的改变[J]. 癌变·畸变·突变, 2017, 29:411-417.]
[19] Filipe EC, Chitty JL, Cox TR. Charting the unexplored extracellular matrix in cancer[J]. Int J Exp Pathol, 2018, 99:58-76.
[20] Kim SH, Turnbull J, Guimond S. Extracellular matrix and cell signalling:the dynamic cooperation of integrin, proteoglycan and growth factor receptor[J]. J Endocrinol, 2011, 209:139-151.
[21] Radisky D, Muschler J, Bissell MJ. Order and disorder:the role of extracellular matrix in epithelial cancer[J]. Cancer Invest, 2002, 20:139-153.
[22] Hanahan D, Coussens LM. Accessories to the crime:functions of cells recruited to the tumor microenvironment[J]. Cancer Cell, 2012, 21:309-322.
[23] Hinz B. The extracellular matrix and transforming growth factor-β 1:tale of a strained relationship[J]. Matrix Biol, 2015, 47:54-65.
[24] Cichon MA, Radisky DC. Extracellular matrix as a contextual determinantof transforming growth factor-β signaling in epithelial-mesenchymal transition and in cancer[J]. Cell Adh Migr, 2014, 8:588-594.
[25] Ungefroren H, Lenschow W, Chen WB, Faendrich F, Kalthoff H. Regulation of biglycan gene expression by transforming growth factor-beta requires MKK6-p38 mitogen-activated protein kinase signaling downstream of Smad signaling[J]. J Biol Chem, 2003, 278:11041-11049.
[26] Verrecchia F, Mauviel A. Transforming growth factor-beta signaling through the Smad pathway:role in extracellular matrix gene expression and regulation[J]. J Invest Dermatol, 2002, 118:211-215.
[27] Wang N, Wang X, Sun B, Zeng M, Xing C, Zhao X, Yang J. Role of TGF-β1 in production of fibronectin in vascular smooth muscle cells cultured under high-phosphate conditions[J]. J Nephrol, 2013, 26:213-218.
[28] Murakami H, Ono K. MELAS:mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes[J]. Brain Nerve, 2017, 69:111-117. |