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Items: 1 to 20 of 140

1.

CaMKII determines mitochondrial stress responses in heart.

Joiner ML, Koval OM, Li J, He BJ, Allamargot C, Gao Z, Luczak ED, Hall DD, Fink BD, Chen B, Yang J, Moore SA, Scholz TD, Strack S, Mohler PJ, Sivitz WI, Song LS, Anderson ME.

Nature. 2012 Nov 8;491(7423):269-73. doi: 10.1038/nature11444. Epub 2012 Oct 10.

2.

Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart.

Rasmussen TP, Wu Y, Joiner ML, Koval OM, Wilson NR, Luczak ED, Wang Q, Chen B, Gao Z, Zhu Z, Wagner BA, Soto J, McCormick ML, Kutschke W, Weiss RM, Yu L, Boudreau RL, Abel ED, Zhan F, Spitz DR, Buettner GR, Song LS, Zingman LV, Anderson ME.

Proc Natl Acad Sci U S A. 2015 Jul 21;112(29):9129-34. doi: 10.1073/pnas.1504705112. Epub 2015 Jul 7.

3.

Distinct mPTP activation mechanisms in ischaemia-reperfusion: contributions of Ca2+, ROS, pH, and inorganic polyphosphate.

Seidlmayer LK, Juettner VV, Kettlewell S, Pavlov EV, Blatter LA, Dedkova EN.

Cardiovasc Res. 2015 May 1;106(2):237-48. doi: 10.1093/cvr/cvv097. Epub 2015 Mar 5.

4.

Local control of mitochondrial membrane potential, permeability transition pore and reactive oxygen species by calcium and calmodulin in rat ventricular myocytes.

Odagiri K, Katoh H, Kawashima H, Tanaka T, Ohtani H, Saotome M, Urushida T, Satoh H, Hayashi H.

J Mol Cell Cardiol. 2009 Jun;46(6):989-97. doi: 10.1016/j.yjmcc.2008.12.022. Epub 2009 Jan 20.

PMID:
19318235
5.

Serine hydrolase inhibitors block necrotic cell death by preventing calcium overload of the mitochondria and permeability transition pore formation.

Yun B, Lee H, Ghosh M, Cravatt BF, Hsu KL, Bonventre JV, Ewing H, Gelb MH, Leslie CC.

J Biol Chem. 2014 Jan 17;289(3):1491-504. doi: 10.1074/jbc.M113.497651. Epub 2013 Dec 2.

6.

The Ca²⁺-calmodulin-Ca²⁺/calmodulin-dependent protein kinase II signaling pathway is involved in oxidative stress-induced mitochondrial permeability transition and apoptosis in isolated rat hepatocytes.

Toledo FD, Pérez LM, Basiglio CL, Ochoa JE, Sanchez Pozzi EJ, Roma MG.

Arch Toxicol. 2014 Sep;88(9):1695-709. doi: 10.1007/s00204-014-1219-5. Epub 2014 Mar 11.

PMID:
24614978
7.

Impact of levosimendan and ischaemia-reperfusion injury on myocardial subsarcolemmal mitochondrial respiratory chain, mitochondrial membrane potential, Ca2+ cycling and ATP synthesis.

Sommer S, Leistner M, Aleksic I, Schimmer C, Alhussini K, Kanofsky P, Leyh RG, Sommer SP.

Eur J Cardiothorac Surg. 2016 Feb;49(2):e54-62; discussion e62. doi: 10.1093/ejcts/ezv397. Epub 2015 Nov 18.

PMID:
26586791
8.

CaMKII (Ca2+/Calmodulin-Dependent Kinase II) in Mitochondria of Smooth Muscle Cells Controls Mitochondrial Mobility, Migration, and Neointima Formation.

Nguyen EK, Koval OM, Noble P, Broadhurst K, Allamargot C, Wu M, Strack S, Thiel WH, Grumbach IM.

Arterioscler Thromb Vasc Biol. 2018 Jun;38(6):1333-1345. doi: 10.1161/ATVBAHA.118.310951. Epub 2018 Mar 29.

9.

Melatonin protects against heart ischemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening.

Petrosillo G, Colantuono G, Moro N, Ruggiero FM, Tiravanti E, Di Venosa N, Fiore T, Paradies G.

Am J Physiol Heart Circ Physiol. 2009 Oct;297(4):H1487-93. doi: 10.1152/ajpheart.00163.2009. Epub 2009 Aug 14.

10.

Mitochondrial PKC-ε deficiency promotes I/R-mediated myocardial injury via GSK3β-dependent mitochondrial permeability transition pore opening.

Wang S, Zhang F, Zhao G, Cheng Y, Wu T, Wu B, Zhang YE.

J Cell Mol Med. 2017 Sep;21(9):2009-2021. doi: 10.1111/jcmm.13121. Epub 2017 Mar 7.

11.

CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis.

Zhang T, Zhang Y, Cui M, Jin L, Wang Y, Lv F, Liu Y, Zheng W, Shang H, Zhang J, Zhang M, Wu H, Guo J, Zhang X, Hu X, Cao CM, Xiao RP.

Nat Med. 2016 Feb;22(2):175-82. doi: 10.1038/nm.4017. Epub 2016 Jan 4.

PMID:
26726877
12.

Heart failure-induced activation of phospholipase iPLA2γ generates hydroxyeicosatetraenoic acids opening the mitochondrial permeability transition pore.

Moon SH, Liu X, Cedars AM, Yang K, Kiebish MA, Joseph SM, Kelley J, Jenkins CM, Gross RW.

J Biol Chem. 2018 Jan 5;293(1):115-129. doi: 10.1074/jbc.RA117.000405. Epub 2017 Nov 20.

13.

Aldose reductase mediates myocardial ischemia-reperfusion injury in part by opening mitochondrial permeability transition pore.

Ananthakrishnan R, Kaneko M, Hwang YC, Quadri N, Gomez T, Li Q, Caspersen C, Ramasamy R.

Am J Physiol Heart Circ Physiol. 2009 Feb;296(2):H333-41. doi: 10.1152/ajpheart.01012.2008. Epub 2008 Dec 5.

14.

Altered FoF1 ATP synthase and susceptibility to mitochondrial permeability transition pore during ischaemia and reperfusion in aging cardiomyocytes.

Fernandez-Sanz C, Ruiz-Meana M, Castellano J, Miro-Casas E, Nuñez E, Inserte J, Vázquez J, Garcia-Dorado D.

Thromb Haemost. 2015 Mar;113(3):441-51. doi: 10.1160/TH14-10-0901. Epub 2015 Jan 29.

PMID:
25631625
15.

Transient opening of mitochondrial permeability transition pore by reactive oxygen species protects myocardium from ischemia-reperfusion injury.

Saotome M, Katoh H, Yaguchi Y, Tanaka T, Urushida T, Satoh H, Hayashi H.

Am J Physiol Heart Circ Physiol. 2009 Apr;296(4):H1125-32. doi: 10.1152/ajpheart.00436.2008. Epub 2009 Feb 6.

16.

Urocortin prevents mitochondrial permeability transition in response to reperfusion injury indirectly by reducing oxidative stress.

Townsend PA, Davidson SM, Clarke SJ, Khaliulin I, Carroll CJ, Scarabelli TM, Knight RA, Stephanou A, Latchman DS, Halestrap AP.

Am J Physiol Heart Circ Physiol. 2007 Aug;293(2):H928-38. Epub 2007 May 4.

17.

HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore.

Ong SG, Lee WH, Theodorou L, Kodo K, Lim SY, Shukla DH, Briston T, Kiriakidis S, Ashcroft M, Davidson SM, Maxwell PH, Yellon DM, Hausenloy DJ.

Cardiovasc Res. 2014 Oct 1;104(1):24-36. doi: 10.1093/cvr/cvu172. Epub 2014 Jul 25.

PMID:
25063991
18.

Calcium-induced cardiac mitochondrial dysfunction is predominantly mediated by cyclosporine A-dependent mitochondrial permeability transition pore.

Yarana C, Sripetchwandee J, Sanit J, Chattipakorn S, Chattipakorn N.

Arch Med Res. 2012 Jul;43(5):333-8. doi: 10.1016/j.arcmed.2012.06.010. Epub 2012 Jul 21.

PMID:
22824212
19.

Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts.

Argaud L, Gateau-Roesch O, Augeul L, Couture-Lepetit E, Loufouat J, Gomez L, Robert D, Ovize M.

Am J Physiol Heart Circ Physiol. 2008 Jan;294(1):H386-91. Epub 2007 Oct 19.

20.

The role of mitochondria in protection of the heart by preconditioning.

Halestrap AP, Clarke SJ, Khaliulin I.

Biochim Biophys Acta. 2007 Aug;1767(8):1007-31. Epub 2007 Jun 2. Review.

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