Mitochondrial function in cardiomyocytes: Target for cardioprotection

Current Opinion in Anaesthesiology

Volumn 18, Issue 1, 2005, Pages 77-82

  Das, Dipak K ^a   Maulik, Nilanjana ^a  

^a UNIVERSITY OF CONNECTICUT SCHOOL OF MEDICINE   (United States)

Author keywords

Akt caspases; Apoptosis; Bax; Bcl 2; Cytochrome C; Mitochondrial permeability transition pore; Mitogen activated protein kinases; Phosphatidylinositol 3 kinase; Reactive oxygen species; Redox signaling

Indexed keywords

IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; PROTEIN BAX; PROTEIN BCL 2; REACTIVE OXYGEN METABOLITE;

BIOENERGY; CELL DEATH; CELL SURVIVAL; HEART MITOCHONDRION; HEART MUSCLE CELL; HEART PROTECTION; HUMAN; NONHUMAN; OXIDATION REDUCTION REACTION; PRIORITY JOURNAL; REVIEW;

EID: 14144250314     PISSN: 09527907     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001503-200502000-00012     Document Type: Review

References (51)

1. Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic cell death are independent contributing variables of infarct size in rats. Lab Invest 1996; 74:86-107.
2. Ray PS, Otani H, Dillmann WH, Das DK. Transgene overexpression of aB-crystallin confers protection against cardiomyocyte apoptosis during myocardial ischemia and reperfusion. FASEB J 2001; 15:393-402. An excellent paper demonstrating that mitochondrial heat shock protein/ antioxidant is involved in cardioprotectiion by inhibiting both apoptosis and necrosis. This paper also describes that both apoptosis and necrosis contribute to myocardial infarction.
3. Bernardi P, Petronilli V, Di Lisa F, Forte M. A mitochondrial perspective on cell death. Trends Biochem Sci 2001; 26:112-117.
4. + and is causative event in the death of myocytes in post-ischemic reperfusion of the heart. J Biol Chem 2001; 276:2571-2575.
5. Gnaiger E, Mendez G, Hand SC. High phosphorylation efficiency and depression of uncoupled respiration in mitochondria under hypoxia. Proc Natl Acad Sci U S A 2000; 97:11080-11085.
6. Das DK, Maulik N. Evaluation of antioxidant effectiveness in ischemia reperfusion tissue injury methods. Methods Enzymol 1994; 233:601-610.
7. Chen Q, Vazquez EJ, Moghaddas S, et al. Production of reactive oxygen species by mitochondria. J Biol Chem 2003; 278:36027-36031. An excellent paper demonstrating that mitochondria are the major source of ROS. The mechanism of the production of ROS is also described in this paper.
8. Shen AC, Jennings RB. Myocardial calcium and magnesium in acute ischemic injury. Am J Pathol 1972; 67:417-421.
9. Liu X, Engelman RM, Wei Z, et al. Attenuation of myocardial reperfusion injury by reducing intracellular calcium overloading with dihydropyridines. Biochem Pharmacol 1993; 45:1333-1341.
10. Prasad MR, Popescu LM, Moraru II, et al. Role of phospholipase A2 and C in myocardial ischemic reperfusion injury. Am J Physiol 1991; 260:H877-H883.
11. Ide T, Tsutsui H, Kinugawa S, et al. Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium. Circ Res 1999; 85:357-363.
12. Esposito LA, Melov S, Panov A, et al. Mitochondrial disease in mouse results in increased oxidative stress. Proc Natl Acad Sci U S A 1999; 96:4820-4825.
13. Takano H, Zou Y, Hasegawa H, et al. Oxidative stress-induced signal transduction pathways in cardiac myocytes: involvement of ROS in heart diseases. Antioxidants Redox Signal 2003; 5:789-794. This paper demonstrates the role of redox signaling in ischemic heart disease.
14. Hattori R, Hernandez TE, Zhu L, et al. An essential role of the antioxidant gene Bcl-2 in myocardial adaptation to ischemia: an insight with antisense Bcl-2 therapy. Antioxidants Redox Signal 2001; 3:403-413.
15. Griendling KK, Sorescu D, Lassegue B, Ushio-Fukai M. Modulation of protein kinase activity and gene expression by reactive oxygen species and their role in vascular physiology and pathophysiology. Arterioscler Thromb Vasc Biol 2000; 20:2175-2183.
16. Das DK. Redox regulation of cardiomyocyte survival and death. Antioxidants Redox Signal 2001; 3:23-37.
17. Narula J, Pandey P, Arbustini E, et al. Apoptosis in heart failure: release of cytochrome C from mitochondria and activation of caspase-3 in human cardiomyopathy. Proc Natl Acad Sci U S A 1999; 96:8144-8149.
18. Tung TC, Cui G, Oshima K, et al. Balanced expression of mitochondrial apoptosis regulatory proteins correlates with long-term survival of cardiac allografts. Am J Physiol 2003; 285:H2832-H2841. This paper reports that cellular injury can potentiate the survival signal through the expression of redox-sensitive proteins.
19. Kim GT, Chun YS, Park JW, Kim MS. Role of apoptosis-inducing factor in myocardial cell death by ischemia-reperfusion. Biochem Biophys Res Commun 2003; 309:619-624.
20. Scheubel RJ, Bartling B, Simm A, et al. Apoptotic pathway activation from mitochondria and death receptors without caspase 3 cleavage in failing human myocardium: fragile balance of myocyte survival? J Am Coll Cardiol 2002; 39:481-488.
21. Li N, Ragheb K, Lawler G, et al. DPI induces mitochondrial superoxide-mediated apoptosis. Free Radic Biol Med 2003; 34:465-477.
22. Yuki K, Miyauchi T, Kakinuma Y, et al. Mitochondrial dysfunction increases expression of endothelin-1 and induces apoptosis through caspase-3 activation in rat cardiomyocytes in vitro. J Cardiovasc Pharmacol 2000; 36 (Suppl. 1):S205-S208.
23. Halestrap AP, Doran E, Gillespie JP, O'Toole A. Mitochondria and cell death. Biochem Soc Trans 2000; 28:170-177.
24. Herrlich P, Bohmer FD. Redox regulation of signal transduction in mammalian cells. Biochem Pharmacol 2000; 59:35-41.
25. Das DK, Maulik N, Sato M, Ray P. Reactive oxygen species function as second messenger during ischemic preconditioning of heart. Mol Cell Biochem 1999; 196:59-67.
26. Maulik N, Goswami S, Galang N, Das DK. Differential regulation of bcl-2, AP-1 and NFκB on cardiomyocyte apoptosis during myocardial ischemic stress adaptation. FEBS Lett 1999; 443:331-336.
27. Maulik N, Sasaki H, Addya S, Das DK. Regulation of cardiomyocyte apoptosis by redox-sensitive transcription factors. FEBS Lett 2000; 485:7-12.
28. Sharma HS, Das DK. Role of cytokines in myocardial ischemia and reperfusion. Mediators Inflamm 1997; 6:175-184.
29. Rosette C, Karin M. Ultraviolet light and osmotic stress: activation of the JNK cascade through multiple growth factor and cytokine receptors. Science 1996; 274:1194-1197.
30. Efimova T, LaCelle P, Welter JF, Eckert RL. Regulation of human involucrin promoter activity by a protein kinase C, Ras, MEKK1, MEK3, p38/RK, AP1 signal transduction pathway. J Biol Chem 1998; 18; 273:24387-24395.
31. Maulik N, Watanabe M, Zu Y-L, et al. Ischemic preconditioning triggers the activation of MAP kinases and MAPKAP kinase 2 in rat hearts. FEBS Lett 1996; 396:233-237.
32. Maulik N, Yoshida T, Zu YL, et al. Ischemic preconditioning triggers tyrosine kinase signaling: a potential role for MAPKAP kinase 2. Am J Physiol 1998; 275:H1857-H1864.
33. Chen Z, Chua CC, Ho YS, et al. Overexpression of Bcl-2 attenuates apoptosis and protects against myocardial I/R injury in transgenic mice. Am J Physiol 2001; 280:H2313-H2320.
34. Nunez G, London L, Hockenbery D, et al. Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived hemopoietic cell lines. J Immunol 1999; 144:3602-3610.
35. Zhang P, Liu B, Kang SW, et al. Thioredoxin peroxidase is a novel inhibitor of apoptosis with a mechanism distinct from that of Bcl-2. J Biol Chem 1997; 272:30615-30618.
36. Gjertsen BT, Logothetis CJ, McDonnell TJ. Molecular regulation of cell death and therapeutic strategies for cell death induction in prostate carcinoma. Cancer Metastas Rev 1998/99; 17:345-351.
37. Maulik N, Engelman RM, Rousou JA, et al. Ischemic preconditioning reduces apoptosis by upregulating anti-death gene bcl-2. Circulation 1999; 100(Suppl. II):369-375.
38. Holmgren A. Thioredoxin. Annu Rev Biochem 1985; 54:237-271.
39. Funasaka Y, Ichihashi M. The effect of ultraviolet B induced adult T cell leukemia-derived factor/thioredoxin (ADF/TRX) on survival and growth of human melanocytes. Pigment Cell Res 1997; 10:68-73.
40. Nakamura H, Vaage J, Valen G, et al. Measurements of plasma glutaredoxin and thioredoxin in healthy volunteers and during open-heart surgery. Free Radic Biol Med 1998; 24:1176-1186.
41. Nimata M, Kishimito C, Shioji K, et al. Upregulation of redox-regulating protein, thioredoxin, in endomyocardial biopsy samples of patients with myocarditis and cardiomyopathies. Mol Cell Biochem 2003; 248:193-196.
42. Nakamura H, Matsuda M, Firuke K, et al. Adult T cell leukemia-derived factor/human thioredoxin protects endothelial F-2 cell injury caused by activated neutrophils or hydrogen peroxide. Immunol Lett 1994; 42:75-80.
43. Korsmeyer SJ. Programmed cell death: Bcl-2. Import Adv Oncol 1993;19-28.
44. Hunter JJ, Bond BL, Parslow TG. Functional dissection of the human Bcl-2 protein: sequence requirements for inhibition of apoptosis. Mol Cell Biol 1996; 16:877-883.
45. Yang E, Zha J, Jockel J, et al. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell 1995; 80:285-291.
46. Narita M, Shimizu S, Ito T, et al. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proc Natl Acad Sci U S A 1998; 95:14681-14686.
47. Goping IS, Gross A, Lavoie JN, et al. Regulated targeting of BAX to mitochondria. J Cell Biol 1998; 143:207-215.
48. Eskes R, Desagher S, Antonsson B, Martinou JC. Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane. Mol Cell Biol 2000; 20:929-935.
49. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 1986; 74:1124-1136.
50. + channel of heart mitochondria. Am J Physiol 2001; 280:H649-H657.
51. Uchiyama T, Engelman RM, Maulik N, Das DK. Role of Akt signaling in mitochondrial survival pathway triggered by hypoxic preconditioning. Circulation 2004; 109:3042-3049.