Mitochondrial cyclophilin-D as a potential therapeutic target for post-myocardial infarction heart failure

Journal of Cellular and Molecular Medicine

Volumn 15, Issue 11, 2011, Pages 2443-2451

  Lim, Shiang Y ^a   Hausenloy, Derek J ^a   Arjun, Sapna ^a   Price, Anthony N ^b   Davidson, Sean M ^a   Lythgoe, Mark F ^b   Yellon, Derek M ^a  

^a ROYAL FREE AND UNIVERSITY COLLEGE MEDICAL SCHOOL   (United Kingdom)

^b UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

Cyclophilin D; Fibrosis; Heart failure; Ischemia

Indexed keywords

CARRIER PROTEIN; CYCLOPHILIN; CYCLOPHILIN D; CYCLOSPORIN; LACTONE; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; SANGLIFEHRIN A; SPIRO COMPOUND;

ANIMAL; APOPTOSIS; ARTICLE; CELL PROLIFERATION; DRUG ANTAGONISM; DRUG EFFECT; GENETICS; HEART FAILURE; HEART INFARCTION; HEART LEFT VENTRICLE FUNCTION; HEART MITOCHONDRION; HEART VENTRICLE; HEART VENTRICLE REMODELING; MALE; METABOLISM; MOUSE; MOUSE MUTANT; PATHOPHYSIOLOGY;

ANIMALS; APOPTOSIS; CELL PROLIFERATION; CYCLOPHILINS; CYCLOSPORINE; HEART FAILURE; HEART VENTRICLES; LACTONES; MALE; MICE; MICE, KNOCKOUT; MITOCHONDRIA, HEART; MITOCHONDRIAL MEMBRANE TRANSPORT PROTEINS; MYOCARDIAL INFARCTION; SPIRO COMPOUNDS; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR FUNCTION, LEFT; VENTRICULAR REMODELING;

MUS;

EID: 80054883388     PISSN: 15821838     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1582-4934.2010.01235.x     Document Type: Article

References (36)

1. Lloyd-Jones D, Adams R, Carnethon M, et al Heart disease and stroke statistics-2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009; 119: e21-181.
2. Ertl G, Frantz S. Healing after myocardial infarction. Cardiovasc Res. 2005; 66: 22-32.
3. Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation. 2000; 101: 2981-8.
4. Baines CP, Kaiser RA, Purcell NH, et al Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death. Nature. 2005; 434: 658-62.
5. Nakagawa T, Shimizu S, Watanabe T, et al Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death. Nature. 2005; 434: 652-8.
6. Hausenloy DJ, Maddock HL, Baxter GF, et al Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning? Cardiovasc Res. 2002; 55: 534-43.
7. Hausenloy DJ, Duchen MR, Yellon DM. Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury. Cardiovasc Res. 2003; 60: 617-25.
8. Argaud L, Gateau-Roesch O, Muntean D, et al Specific inhibition of the mitochondrial permeability transition prevents lethal reperfusion injury. J Mol Cell Cardiol. 2005; 38: 367-74.
9. Piot C, Croisille P, Staat P, et al Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med. 2008; 359: 473-81.
10. Mewton N, Croisille P, Gahide G, et al Effect of cyclosporine on left ventricular remodeling after reperfused myocardial infarction. J Am Coll Cardiol. 2010; 55: 1200-5.
11. Kumaran C, Shivakumar K. Calcium- and superoxide anion-mediated mitogenic action of substance P on cardiac fibroblasts. Am J Physiol Heart Circ Physiol. 2002; 282: H1855-62.
12. Goldsmith EC, Hoffman A, Morales MO, et al Organization of fibroblasts in the heart. Dev Dyn. 2004; 230: 787-94.
13. Sharov VG, Todor A, Khanal S, et al Cyclosporine A attenuates mitochondrial permeability transition and improves mitochondrial respiratory function in cardiomyocytes isolated from dogs with heart failure. J Mol Cell Cardiol. 2007; 42: 150-8.
14. Sharov VG, Todor AV, Imai M, et al Inhibition of mitochondrial permeability transition pores by cyclosporine A improves cytochrome C oxidase function and increases rate of ATP synthesis in failing cardiomyocytes. Heart Fail Rev. 2005; 10: 305-10.
15. Javadov S, Baetz D, Rajapurohitam V, et al Antihypertrophic effect of Na+/H+ exchanger isoform 1 inhibition is mediated by reduced mitogen-activated protein kinase activation secondary to improved mitochondrial integrity and decreased generation of mitochondrial-derived reactive oxygen species. J Pharmacol Exp Ther. 2006; 317: 1036-43.
16. Leshnower BG, Kanemoto S, Matsubara M, et al Cyclosporine preserves mitochondrial morphology after myocardial ischemia/reperfusion independent of calcineurin inhibition. Ann Thorac Surg. 2008; 86: 1286-92.
17. Minners J, van den Bos EJ, Yellon DM, et al Dinitrophenol, cyclosporin A, and trimetazidine modulate preconditioning in the isolated rat heart: support for a mitochondrial role in cardioprotection. Cardiovasc Res. 2000; 47: 68-73.
18. Cereghetti GM, Stangherlin A, Martins dB, et al Dephosphorylation by calcineurin regulates translocation of Drp1 to mitochondria. Proc Natl Acad Sci USA. 2008; 105: 15803-8.
19. Nakayama H, Chen X, Baines CP, et al Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure. J Clin Invest. 2007; 117: 2431-44.
20. Tao ZY, Cavasin MA, Yang F, et al Temporal changes in matrix metalloproteinase expression and inflammatory response associated with cardiac rupture after myocardial infarction in mice. Life Sci. 2004; 74: 1561-72.
21. Gao XM, Xu Q, Kiriazis H, et al Mouse model of post-infarct ventricular rupture: time course, strain- and gender-dependency, tensile strength, and histopathology. Cardiovasc Res. 2005; 65: 469-77.
22. Fang L, Gao XM, Moore XL, et al Differences in inflammation, MMP activation and collagen damage account for gender difference in murine cardiac rupture following myocardial infarction. J Mol Cell Cardiol. 2007; 43: 535-44.
23. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system. Circulation. 1991; 83: 1849-65.
24. Swynghedauw B. Molecular mechanisms of myocardial remodeling. Physiol Rev. 1999; 79: 215-62.
25. Sun Y. Myocardial repair/remodelling following infarction: roles of local factors. Cardiovasc Res. 2009; 81: 482-90.
26. Yin FC, Spurgeon HA, Rakusan K, et al Use of tibial length to quantify cardiac hypertrophy: application in the aging rat. Am J Physiol. 1982; 243: H941-7.
27. Bartling B, Holtz J, Darmer D. Contribution of myocyte apoptosis to myocardial infarction? Basic Res Cardiol. 1998; 93: 71-84.
28. Sam F, Sawyer DB, Chang DL, et al Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart. Am J Physiol Heart Circ Physiol. 2000; 279: H422-8.
29. Cleutjens JP, Blankesteijn WM, Daemen MJ, et al The infarcted myocardium: simply dead tissue, or a lively target for therapeutic interventions. Cardiovasc Res. 1999; 44: 232-41.
30. Eliseev RA, Malecki J, Lester T, et al Cyclophilin D interacts with Bcl2 and exerts an anti-apoptotic effect. J Biol Chem. 2009; 284: 9692-9.
31. Forte M, Bernardi P. The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents? Cell Death Differ. 2006; 13: 1287-90.
32. Palma E, Tiepolo T, Angelin A, et al Genetic ablation of cyclophilin D rescues mitochondrial defects and prevents muscle apoptosis in collagen VI myopathic mice. Hum Mol Genet. 2009; 18: 2024-31.
33. Gomez L, Thibault H, Gharib A, et al Inhibition of mitochondrial permeability transition improves functional recovery and reduces mortality following acute myocardial infarction in mice. Am J Physiol Heart Circ Physiol. 2007; 293: H1654-61.
34. Bagci G, Yucel I, Duranoglu Y. The effect of cyclosporin A on cultured rabbit subconjunctival fibroblast proliferation. Ophthalmologica. 1999; 213: 114-9.
35. Johnsson C, Gerdin B, Tufveson G. Effects of commonly used immunosuppressants on graft-derived fibroblasts. Clin Exp Immunol. 2004; 136: 405-12.
36. Yamada H, Nishimura F, Naruishi K, et al Phenytoin and cyclosporin A suppress the expression of MMP-1, TIMP-1, and cathepsin L, but not cathepsin B in cultured gingival fibroblasts. J Periodontol. 2000; 71: 955-60.