137
Views
31
CrossRef citations to date
0
Altmetric
Miscellaneous

Therapeutic potential of CPT I inhibitors: cardiac gene transcription as a target

&
Pages 345-356 | Published online: 24 Feb 2005

Bibliography

  • TUTWILER GF, RYZLAK MT: Inhibition of mitochondrial carnitine palmitoyl transferase by 2-tetradecylglycidic acid (McN-3802) (preliminary communication). Life Sri. (1980) 26:393–397.
  • EISTETTER K, WOLF HP: Synthesis and hypoglycemic activity of phenylalkylwdranecarboxylic acid derivatives. Med. Chem. (1982) 25:109–113.
  • WOLF HP, ENGEL DW: Decrease of fatty acid oxidation, ketogenesis and gluconeogenesis in isolated perfused rat liver by phenylalkyl oxirane carboxylate (B 807-27) due to inhibition of CPT I (EC 2.3.1.21). Eur. Biochein. (1985) 146:359–363.
  • SCHMITZ FJ, ROSEN P, REINAUER H: Improvement of myocardial function and metabolism in diabetic rats by the carnitine palmitoyl transferase inhibitor Etomwdr. Henn. Metab. Res. (1995) 27:515–522.
  • HUBINGER A, KNODE 0, SUSANTO F et al.: Effects of the carnitine-acyltransferase inhibitor etomoxir on insulin sensitivity, energy expenditure and substrate oxidation in NIDDM. Horin. Metab. Res. (1997) 29:436–439.
  • ARONOFF S, ROSENBLATT S, BRAITHWAITE S et al.: Pioglitazone hydrochloride monotherapy improves glycemic control in the treatment of patients with Type 2 diabetes: a 6-month randomized placebo-controlled dose-response study. The Pioglitazone 001 Study Group. Diabetes Care (2000) 23:1605–1611.
  • DEEMS RO, ANDERSON RC, FOLEY JE: Hypoglycemic effects of a novel fatty acid oxidation inhibitor in rats and monkeys. Am. .1. Physic] (1998) 274:R524–R528.
  • YOTSUMOTO T, NAITOH T, KITAHARA M et al.: Effects of carnitine palmitoyltransferase I inhibitors on hepatic hypertrophy. Eur. I Phannacol (2000) 398:297–302.
  • ZARAIN-HERZBERG A, RUPP H: Transcriptional modulators targeted at fuel metabolism of hypertrophied heart. Am. .1. Cardiel (1999) 83:31H–37H.
  • SCHMIDT-SCHWEDA S, HOLUBARSCH C: First clinical trial with etomoxir in patients with chronic congestive heart failure. Clin. Sci. (Colch) (2000) 99:27–35.
  • ••First clinical trial with etomoxir in heartfailure patients.
  • BRISTOW M: Etomoxir: a new approach to treatment of chronic heart failure. Lancet (2000) 356:1621–1622.
  • ••Editorial discussing etomoxir as a new approach to heart failure treatment.
  • BEAMISH RE: Heart failure: the ironic failure of success. Can. Cardiol (1994) 10:603.
  • MORKIN E: Control of cardiac myosin heavy chain gene expression. Microsc. Res. Tech. (2000) 50:522–531.
  • DILLMANN WH: Calcium regulatory proteins and their alteration by transgenic approaches. Am. .1. Cardiol (1999) 83:89H–91H.
  • PERIASAMY M, HUKE S: SERCA pump level is a critical determinant of Ca(2+)homeostasis and cardiac contractility. J. Ma Cell Cardiol (2001) 33:1053–1063.
  • RUPP H: Diastolic dysfunction of the heart: pharmacological strategies for modulating calcium sequestration of the sarcoplasmic reticulum. In: Heart function in health and disease. B Ostadal, NS Dhalla (Eds.) Kluwer Academic Publishers, Boston, USA (1993):251–271.
  • AGGARWAL A, BROWN KA, LEWINTER MM: Diastolic dysfunction: pathophysiology, clinical features and assessment with radionuclide methods. Nucl. Cardiol (2001) 8:98–106.
  • HASENFUSS G, REINECKE H, STUDER R et al.: Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium. Circ. Res. (1994) 75:434–442.
  • ••Study demonstrates link between SERCA2expression and function of human heart.
  • RUPP H, VETTER R: Sarcoplasmic reticulum function and carnitine palmitoyltransferase-1 inhibition during progression of heart failure. Br. Pharmacol (2000) 131:1748–1756.
  • KINUGAWA K, MINOBE WA, WOOD WM et al.: Signaling pathways responsible for fetal gene induction in the failing human heart : evidence for altered thyroid hormone receptor gene expression. Circulation (2001) 103:1089–1094.
  • KINUGAWA K, YONEKURA K, RIBEIRO RC et al.: Regulation of thyroid hormone receptor isoforms in physiological and pathological cardiac hypertrophy. Circ. Res. (2001) 89:591–598.
  • MORKIN E, PENNOCK GD, RAYA TE et al.: Development of a thyroid hormone analogue for the treatment of congestive heart failure. Thyroid (1996) 6:521–526.
  • PENNOCK GD, SPOONER PH, SUMMERS CE et al: Prevention of abnormal sarcoplasmic reticulum calcium transport and protein expression in post-infarction heart failure using 3, 5-diiodothyropropionic acid (DITPA)..1. Cell Cardiol (2000) 32:1939–1953.
  • RUPP H, WAHL R, JACOB R: Remodelling of the myocyte at a molecular level - relationship between myosin isozyme population and sarcoplasmic reticulum. In: Heart function and metabolism. NS Dhalla, GN Pierce, RE Beamish (Eds.) Martinus Nijhoff Publishing, Boston, USA (1987):307–318.
  • RUPP H, ELIMBAN V, DHALLA NS: Diabetes-like action of intermittent fasting on sarcoplasmic reticulum Ca2+-pump ATPase and myosin isoenzymes can be prevented by sucrose. Biochem. Biophys. Res. Commun. (1989) 164:319–325.
  • FUKASE N, TAKAHASHI H, MANAKA H et al.: Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion. Diabetes Res. Clin. Pract. (1992) 15:187–195.
  • RUPP H, ELIMBAN V, DHALLA NS: Sucrose feeding prevents changes in myosin isoenzymes and sarcoplasmic reticulum Ca2+-pump ATPase in pressure-loaded rat heart. Biochem. Biophys. Res. Commun. (1988) 156:917–923.
  • RUPP H, WAHL R, HANSEN M: Influence of diet and carnitine palmitoyltransferase I inhibition on myosin and sarcoplasmic reticulum. 1 Appl Physiol (1992) 72:352–360.
  • ••First study showing that etomoxir increasesCa2+ uptake rate of SR.
  • RUPP H, ELIMBAN V, DHALLA NS: Modification of subcellular organelles in pressure-overloaded heart by etomoxir, a carnitine palmitoyltransferase I inhibitor. FASEB (1992) 6:2349–2353.
  • VETTER R, RUPP H: CPT-1 inhibition by etomoxir has a chamber-related action on cardiac sarcoplasmic reticulum and isomyosins. Am. Physiol (1994) 267:H2091–H2099.
  • RUPP H, SCHULZE W, VETTER R: Dietary medium-chain triglycerides can prevent changes in myosin and SR due to CPT-1 inhibition by etomoxir. Am. I Physiol (1995) 269:R630–R640.
  • ZARAIN-HERZBERG A, RUPP H, ELIMBAN V et al.: Modification of sarcoplasmic reticulum gene expression in pressure overload cardiac hypertrophy by etomoxir. FASEB J. (1996) 10:1303–1309.
  • ••Etomoxir increases SERCA2 mRNA abundance in overloaded hearts.
  • VETTER R, KOTT M, RUPP H: Differential influences of carnitine palmitoyltransferase-1 inhibition and hyperthyroidism on cardiac growth and sarcoplasmic reticulum phosphorylation. Eur. Heart .1. (1995) 16(Suppl. C):15–19.
  • TURCANI M, RUPP H: Etomoxir improves left ventricular performance of pressure-overloaded rat heart. Circulation (1997) 96:3681–3686.
  • ••Etomoxir increases selectively the functionof overloaded hearts.
  • RUPP H, ELIMBAN V, DHALLA NS: Differential influence of fasting and BM13.907 treatment on growth and phenotype of pressure overloaded rat heart. MM. Cell Biochem. (1998) 188:209–215.
  • PORTILLA D, DAI G, PETERS JM et al.:Etomoxir-induced PPARcc-modulated enzymes protect during acute renal failure. Am. I Physiol Renal Physiol (2000) 278:F667–F675.
  • BARGER PM, BRANDT JM, LEONE TC et al.: Deactivation of peroxisome proliferator-activated receptor-a during cardiac hypertrophic growth. I. Clin. Invest (2000) 105:1723–1730.
  • DILLMANN WH: Diabetes mellitus and hypothyroidism induce changes in myosin isoenzyme distribution in the rat heart--do alterations in fuel flux mediate these changes? Adv. Exp. Med. Biol. (1986) 194:469–479.
  • SELBY PL, SHERRATT HS: Substituted 2-wdranecarboxylic acids: a new group of candidate hypoglycaemic drugs. Trends Pharmacol Sci. (1989) 10:495–500.
  • LYTTON J, ZARAIN-HERZBERG A, PERIASAMY M et al.: Molecular cloning of the mammalian smooth muscle sarco(endo)plasmic reticulum Ca2+-ATPase. Biol. Chem. (1989) 264:7059–7065.
  • ZARAIN-HERZBERG A, MACLENNAN DH, PERIASAMY M: Characterization of rabbit cardiac sarco(endo)plasmic reticulum Ca2+-ATPase gene. I Biol. Chem. (1990) 265:4670–4677.
  • ROHRER DK, HARTONG R, DILLMANN WH: Influence of thyroid hormone and retinoic acid on slow sarcoplasmic reticulum Ca2+-ATPase and myosin heavy chain alpha gene expression in cardiac myocytes. Delineation of cis-active DNA elements that confer responsiveness to thyroid hormone but not to retinoic acid. I. Biol. Chem. (1991) 266:8638–8646.
  • ••
  • ••
  • WANKERL M, BOHELER KR, FISZMAN MY et al.: Molecular cloning of the human cardiac sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2) gene promoter. Moi Cell Cardiol. (1996) 28:2139–2150.
  • VER HEYEN M, REED TD, BLOUGH RI et al.: Structure and organization of the mouse Atp2a2 gene encoding the sarco(endo)plasmic reticulum Ca2+-ATPase 2 (SERCA2) isoforms. Marnm. Cenoine (2000) 11:159–163.
  • BAKER DL, DAVE V, REED T, PERIASAMY M: Multiple Spl binding sites in the cardiac-slow twitch muscle sarcoplasmic reticulum Ca2+-ATPase gene promoter are required for expression in So18 muscle cells., " Biol. Chem. (1996) 271:5921–5928.
  • BAKER DL, DAVE V, REED T et al: A novel E box/AT-rich element is required for muscle-specific expression of the sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene. Nucleic Acids Res. (1998) 26:1092–1098.
  • ARAI M, YOGUCHI A, TAKIZAWA T et al.: Mechanism of doxorubicin-induced inhibition of sarcoplasmic reticulum Ca(2+)-ATPase gene transcription. Circ. Res. (2000) 86:8–14.
  • SAADANE N, ALPERT L, CHALIFOUR LE: TAFI1250, Egr-1 and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin. Am. J. Physiol (1999) 276:H803–H814.
  • GASHLER A, SUKHATME VP: Early growth response protein 1 (Egr-1): prototype of a zinc-finger family of transcription factors. Frog. Nucleic Add Res. Ma Biol. (1995) 50:191–224.
  • SACK MN, DISCH DL, ROCKMAN HA et al.:A role for Sp and nuclear receptor transcription factors in a cardiac hypertrophic growth program. Proc. Nati Acad. Sci. USA (1997) 94:6438–6443.
  • SHIMOYAMA M, HAYASHI D, TAKIMOTO E et al.: Calcineurin plays a critical role in pressure overload-induced cardiac hypertrophy. Circulation (1999) 100:2449–2454.
  • ZOU Y, HIROI Y, UOZUMI H et al.: Calcineurin plays a critical role in the development of pressure overload-induced cardiac hypertrophy. Circulation (2001) 104:97–101.
  • ZARAIN-HERZBERG A, MARQUES J, SUKOVICH D et al.: Thyroid hormone receptor modulates the expression of the rabbit cardiac sarco (endo) plasmic reticulum Ca2+-ATPase gene. J. Biol. Chem. (1994) 269:1460–1467.
  • ••The first demonstration that thyroidhormome receptor regulates the transcription of the SERCA2 gene.
  • HARTONG R, WANG N, KUROKAWA R et al.: Delineation of three different thyroid hormone-response elements in promoter of rat sarcoplasmic reticulum Ca2+-ATPase gene. Demonstration that retinoid X receptor binds 5' to thyroid hormone receptor in response element 1.1 Biol. Chem. (1994) 269:13021–13029.
  • MORISCOT AS, SAYEN MR, HARTONGR, WU P et al.: Transcription of the rat sarcoplasmic reticulum Ca2±-adenosine triphosphatase gene is increased by 3,5,3'-triiodothyronine receptor isoform-specific interactions with the myocyte-specific enhancer factor-2a. Endocrinology (1997) 138:26–32.
  • LEHNART SE, SCHILLINGER W, PIESKE B et al: Sarcoplasmic reticulum proteins in heart failure. Ann. NY Acad. Sci. (1998) 853:220–230.
  • QI M, SHANNON TR, EULER DE et al.: Down regulation of the sarcoplasmic reticulum Ca2+-ATPase during progression of left ventricular hypertrophy. Am. .1. Physiol. (1997) 41:H2416–H2424.
  • RIBADEAU DA, WISNEWSKY C, BOHELER KR et aL: The sarco(endo)plasmic reticulum Ca2+-ATPase gene is regulated at the transcriptional level during compensated left ventricular hypertrophy in the rat. C R Acad. Sci. III (1997) 320:963–969.
  • TAKIZAWA T, ARAI M, YOGUCHI A et al.: Transcription of the SERCA2 gene is decreased in pressure-overloaded hearts: A study using in vivo direct gene transfer into living myocardium.i. Ma Cell Cardiol. (1999) 12:2167–2174.
  • ••First demonstration that the SERCA2 genetranscription is down-regulated in pressure-overloaded rat hearts.
  • AOYAGI T, YONEKURA K, ETO Yet aL:The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene promoter activity is decreased in response to severe left ventricular pressure-overload hypertrophy in rat hearts. j. Ma Cell Cardiol. (1999) 4:919–926.
  • TAKIZAWA T, ARAI M, TOMARU K et aL: Transcription factor Spl is critical for the transcriptional activity of sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene in pressure-overloaded heart: A study using in vivo direct gene transfer into living myocardium. Circulation (2001) 104:11–137.
  • ANDREWS C, HO PD, DILLMANN WH et al.: Activation of the MKK6-p38-MAPK pathway in cardiac myocytes prolongs the decay phase of the contractile calcium transient, downregulates SERCA2 expression and activates NF-AT-dependent gene expression in contraction-dependent manner. Circulation (2001) 104:11–136.
  • BARGER PM, KELLY DP: PPAR signalingin the control of cardiac energy metabolism. Trends Cardiovasc. Med. (2000) 10:238–245.
  • BARGER PM, BROWNING AC, GARNER AN et al: p38 Mitogen-activated Protein Kinase Activates Perwdsome Proliferator-activated Receptor alpha. A potential role in the cardiac metabolic stress response.j Biol. Chem. (2001) 276:44495–44501.
  • ZEMEL MB, KIM Y-C: Insulin stimulation of intracellular free Ca2+ recovery and Ca2+-ATPase gene expression in cultured vascular smooth-muscle cells: role of glucose-6-phosphate. Biochem. J. (1995) 311:555–559.
  • VAN DER LEE KA, VORK MM, DE VRIES JE et al.: Long-chain fatty acid-induced changes in gene expression in neonatal cardiac myocytes. J. Lipid Res. (2000) 41:41–47.
  • OJAMAA K, SAMAREL AM, KLEIN I: Identification of a contractile-responsive element in the cardiac alpha-myosin heavy chain gene., " Biol. Chem. (1995) 270:31276–31281.
  • XIAO Q, OJAMAA K: Regulation of cardiacalpha-myosin heavy chain gene transcription by a contractile-responsive E-box binding protein., " Ma Cell Cardiol. (1998) 30:87–95.
  • SHEER D, MORKIN E: Myosin isoenzyme expression in rat ventricle: effects of thyroid hormone analogs, catecholamines, glucocorticoids and high carbohydrate diet." Pharmacol Exp. Ther. (1984) 229:872–879.
  • DILLMANN WH: Myosin isoenzyme distribution and Ca+2-activated myosin ATPase activity in the rat heart is influenced by fructose feeding and triiodothyronine. Endocrinology(1985) 116:2160–2166.
  • YOSHIDA H, OKADA T, HAZE K et al.: Endoplasmic reticulum stress-induced formation of transcription factor complex ERSF including NF-Y (CBF) and activating transcription factors 6alpha and 6beta that activates the mammalian unfolded protein response. Ma Cell Biol. (2001) 21:1239–1248.
  • BARNES JA, SMOAK IW: Glucose-regulated protein 78 (GRP78) is elevated in embryonic mouse heart and induced following hypoglycemic stress. Anat. Embryo]. (Ben) (2000) 202:67–74.
  • CASPERSEN C, PEDERSEN PS, TREIMAN M: The sarco/endoplasmic reticulum calcium-ATPase 26 is an endoplasmic reticulum stress-inducible protein. Biol. Chem. (2000) 275:22363–22372.
  • WU KD, BUNGARD D, LYTTON J: Regulation of SERCA Ca2+ pump expression by cytoplasmic Ca2+ in vascular smooth muscle cells. Am. J. Physic] Cell Physic] (2001) 280:C843–C851.
  • THUERAUF DJ, HOOVER H, MELLERJ et al.: Sarco/endoplasmic reticulum calcium ATPase-2 (SERCA2) expression is regulated by ATF6 during the endoplasmic reticulum stress response: Intracellular signaling of calcium stress in a cardiac myocyte model system. Biol. Chem. (2001) 276: 48309–48317.
  • ••First demonstration that SERCA2 genetranscription is regulated by ATF6 during ER stress response.
  • YOUNG ME, LAWS FA, GOODWIN GW, TAEGTMEYER H: Reactivation of perwdsome proliferator-activated receptor alpha is associated with contractile dysfunction in hypertrophied rat heart. I. Biol. Chem. (2001) 276:44390–44395.
  • VAN BILSEN M, VAN DER VUSSE GJ, RENEMAN RS: Transcriptional regulation of metabolic processes: implications for cardiac metabolism. Pflugers Arch. (1998) 437:2–14.
  • ••Overview on metabolically regulated geneexpression.
  • TAEGTMEYER H: Genetics of energetics: transcriptional responses in cardiac metabolism. Ann. Biomed. Eng. (2000) 28:871–876.
  • ••Overview on metabolically regulated geneexpression.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.