For instance, p38 has been proven to phosphorylate glycogen synthase kinase 3 as well as the Wnt signalling pathways (Bikkavilli et?al

For instance, p38 has been proven to phosphorylate glycogen synthase kinase 3 as well as the Wnt signalling pathways (Bikkavilli et?al., 2008; Thornton et?al., 2008). we will summarize the full total outcomes of recent cardiovascular clinical studies with p38 inhibitors. Desks of Links to become phosphorylated by and isoforms just (Cuenda (Parker homologue of p38 may be the pheromone and stress-sensing gene (Bell is normally a component within a hierarchical activation cascade and it is turned on by phosphorylation of its activation loop theme with the upstream kinases, Pbs2 (Brewster and rat style of diabetes by administration of streptozotocin in the current presence of SB239063.SB239063 attenuated diabetes-induced p38 phosphorylation and improved impairments in LV and endothelial function.Widder MRI assessment of ApoE?/? mouse aortas with SB239063 and AngII.SB239063 inhibited p38 activity, irritation in atherosclerotic plaques and phagocytic activity of macrophages and reduced aortic main lesion size.Platelet activationAlrehani and aPL-induced monocyte adherence to HUVEC and respectively.LPS infusion enhanced p38 phosphorylation and TxA2 creation in leukocytes and platelets. SB203580 attenuated LPS-induced TxA2 discharge in platelets.Sakurai pig style of ischaemic preconditioning by LAD ligation (regional ischaemia).IP boosts co-localization of p38 with Cx43 and preserves phosphorylation of Cx43 during ischaemia. Inhibition of p38MAPK by SB203580 attenuated IP-induced IS-reduction and resulted in dephosphorylation of Cx43 that correlates using the propagation of I/R damage.Sanada canine style of ischaemic preconditioning by coronary occlusion (regional ischaemia).p38 MAPK activation during IP mediates the cardioprotection accompanied by HSP27 phosphorylation/translocation mainly. SB203580 treatment during IP blunted the infarct size restriction by IP and attenuated phosphorylation/translocation of HSP27.Marais et?al., 2001Langendorff-perfused rat hearts put through global ischaemia- reperfusion and cultured rat neonatal cardiac myocytesp38 was turned on during preconditioning and attenuated during following ischaemia. Non-preconditioned hearts acquired raised p38 activation compared. p38 inhibition by SB203580 during reperfusion and ischaemia is cardioprotective.Saurin et?al., 2000Ectopic appearance p38 or p38 isoforms in cultured rat neonatal cardiac myocytes put through simulated ischaemia in the current presence of SB203580.Inhibition of p38 during prolonged ischaemia reduced damage and contributed to preconditioning-induced cardioprotection.p38 and p38 activated or deactivated respectively differentially, during ischaemia.Nagarkatti et?al., 1998Simulated ischaemia in rat myoblast cell series H9c2.Inhibition of p38 prior to the starting point of SI blocks preconditioning, but is protective during prolonged ischaemia.Weinbrenner et?al., 1997Langendorff-perfused rabbit hearts put through global ischaemia-reperfusion in existence of SB203580Inhibition of p38 activation abolished security in preconditioned hearts and cardiomyocytes.Tong et?al., 2000Langendorff-perfused rat hearts, preconditioned with or without SB202190Preconditioning induced uptake of blood sugar was abrogated by the current presence of SB202190 Open up in another screen AEA, anandamide; ANF, atrial natriuretic peptide; AP, actions potentials; aPL, antiphospholipid antibodies; ApoE, apolipoprotein E; AngII, angiotensin II; bFGF, simple fibroblast growth aspect; CTGF, connective tissues growth aspect; Ctsk, cathepsin K; Cx43, difference junction proteins connexin43; DN, prominent detrimental; FGF, fibroblast development aspect; GlcNAc, N-acetylglucosamine; H9c2, rat myoblast cell series; Hcy, homocysteine; HHcy, hyperhomocysteinaemia; ICAM, intercellular cell adhesion molecule; IP, ischaemic preconditioning; I/R, ischaemia/reperfusion; Is normally, infarct size; ISO, isoproterenol; LAD, still left anterior descending coronary artery; LV, still left ventricle; MAPKAPK2, MAPK turned on PK 2; MI, myocardial infarction; MMP, matrix metalloproteinase; NADPH, nicotinamide adenine dinucleotide phosphate; NFAT, nuclear aspect of turned on T-cell; Npc1, NiemannCPick disease type C1; PCADK, poly(cyclohexane-1,4-diyl acetone dimethylene ketal); PE, phenylephrine; PEG-SOD, polyethylene glycol superoxide dismutase; PV, pulmonary vein; ROS, reactive air types; SB, SB203580; SERCA2, sarcoplasmic reticulum Ca2+ ATPase; SI, simulated ischaemia; SMA, even muscles actin; SMC, even muscles cell; TAC, transverse aortic constriction; TLR, Toll-like receptor; TxA2, thromboxane A2; WT, outrageous type. The results that p38 activation aggravates many the different parts of atherothrombosis and myocardial infarction, possess laid the building blocks for.SOLSTICE was a GlaxoSmithKline-sponsored stage 2 research performed with the Duke Clinical Analysis Institute (“type”:”clinical-trial”,”attrs”:”text”:”NCT00910962″,”term_id”:”NCT00910962″NCT00910962) (Newby et?al., 2014). transduce extracellular alerts and organize the cellular responses necessary for success and adaptation. However, in various other and coronary disease state governments, these same systems can cause maladaptive replies that aggravate, than alleviate rather, the disease. This example is normally analogous to adrenergic, aldosterone and angiotensin signalling in center failing, where inhibition is effective inspite of the need for these human hormones to homeostasis. The relevant question is whether similar benefits could accrue from p38 inhibition? Within this review, we will discuss the function and framework of p38, days gone by history of p38 inhibitors and their use in preclinical studies. Finally, we will summarize the outcomes of latest cardiovascular clinical studies with p38 inhibitors. Desks of Links to become phosphorylated by and isoforms just (Cuenda (Parker homologue of p38 may be the pheromone and stress-sensing gene (Bell is normally a component within a hierarchical activation cascade and it is turned on by phosphorylation of its activation loop theme with the upstream kinases, Pbs2 (Brewster and rat style of diabetes by administration of streptozotocin in the current presence of SB239063.SB239063 attenuated diabetes-induced p38 phosphorylation and improved impairments in LV and endothelial function.Widder MRI assessment of ApoE?/? mouse aortas with AngII and SB239063.SB239063 inhibited p38 activity, irritation in atherosclerotic plaques and phagocytic activity of macrophages and reduced aortic main lesion size.Platelet activationAlrehani and aPL-induced monocyte adherence to HUVEC and respectively.LPS infusion enhanced p38 phosphorylation and TxA2 creation in platelets and leukocytes. SB203580 attenuated LPS-induced TxA2 discharge in platelets.Sakurai pig style of ischaemic preconditioning by LAD ligation (regional ischaemia).IP boosts co-localization of p38 with Cx43 and preserves phosphorylation of Cx43 during ischaemia. Inhibition of p38MAPK by SB203580 attenuated IP-induced IS-reduction and resulted in dephosphorylation of Cx43 that Nomilin correlates using the propagation of I/R damage.Sanada canine style of ischaemic preconditioning by coronary occlusion (regional ischaemia).p38 MAPK activation during IP mainly mediates the cardioprotection accompanied by HSP27 phosphorylation/translocation. SB203580 treatment during IP blunted the infarct size restriction by IP and attenuated phosphorylation/translocation of HSP27.Marais et?al., 2001Langendorff-perfused rat hearts put through global ischaemia- reperfusion and cultured rat neonatal cardiac myocytesp38 was turned on during preconditioning and attenuated during following ischaemia. Non-preconditioned hearts acquired raised p38 activation compared. p38 inhibition by SB203580 during ischaemia and reperfusion is normally cardioprotective.Saurin et?al., 2000Ectopic appearance p38 or p38 isoforms in cultured rat neonatal cardiac myocytes put through simulated ischaemia in the current presence of SB203580.Inhibition of p38 during prolonged ischaemia reduced damage and contributed to preconditioning-induced cardioprotection.p38 and p38 differentially activated or deactivated respectively, during ischaemia.Nagarkatti et?al., 1998Simulated ischaemia in rat myoblast cell series H9c2.Inhibition of p38 prior to the starting point of SI blocks preconditioning, but is protective during prolonged ischaemia.Weinbrenner et?al., 1997Langendorff-perfused rabbit hearts put through global ischaemia-reperfusion in existence of SB203580Inhibition of p38 activation abolished security in preconditioned hearts and cardiomyocytes.Tong et?al., 2000Langendorff-perfused rat hearts, preconditioned with or without SB202190Preconditioning induced uptake of blood sugar was abrogated by the current presence of SB202190 Open up in another screen AEA, anandamide; ANF, atrial natriuretic peptide; AP, actions potentials; aPL, antiphospholipid antibodies; ApoE, apolipoprotein E; AngII, angiotensin II; bFGF, simple fibroblast growth aspect; CTGF, connective tissues growth aspect; Ctsk, cathepsin K; Cx43, difference junction proteins connexin43; DN, prominent detrimental; FGF, fibroblast development aspect; GlcNAc, N-acetylglucosamine; H9c2, rat myoblast cell series; Hcy, homocysteine; HHcy, hyperhomocysteinaemia; ICAM, intercellular cell adhesion molecule; IP, ischaemic preconditioning; I/R, ischaemia/reperfusion; Is normally, infarct size; ISO, isoproterenol; LAD, still left anterior descending coronary artery; LV, still left ventricle; MAPKAPK2, MAPK turned on PK 2; MI, myocardial infarction; MMP, matrix metalloproteinase; NADPH, nicotinamide adenine dinucleotide phosphate; NFAT, nuclear aspect of turned on T-cell; Npc1, NiemannCPick disease type C1; PCADK, poly(cyclohexane-1,4-diyl acetone dimethylene ketal); PE, phenylephrine; PEG-SOD, polyethylene glycol superoxide dismutase; PV, pulmonary vein; ROS, reactive air types; SB, SB203580; SERCA2, sarcoplasmic reticulum Ca2+ ATPase; SI, simulated ischaemia; SMA, even muscles actin; SMC, even muscles cell; TAC, transverse aortic constriction; TLR, Toll-like receptor; TxA2, thromboxane A2; WT, outrageous type. The results that p38 activation aggravates many the different parts of atherothrombosis and myocardial infarction, possess laid the building blocks for relevant and latest clinical trial activity. The firms with realtors under investigation consist of GlaxoSmithKline (losmapimod, several studies), ArrayBioPharma (ARRY-371797, “type”:”clinical-trial”,”attrs”:”text”:”NCT02057341″,”term_id”:”NCT02057341″NCT02057341) and Bristol-Myers Squibb.A recently available paper in addition has indicated p38 might take part in multiprotein organic hypertrophy mediated with a PKA anchoring proteins, in conjunction with MKK3. and function of p38, the annals of p38 inhibitors and their make use of in preclinical research. Finally, we will summarize the outcomes of latest cardiovascular clinical Nomilin studies with p38 inhibitors. Desks of Links to become phosphorylated by and isoforms just (Cuenda (Parker homologue of p38 may be the pheromone and stress-sensing gene (Bell is normally a component within a hierarchical activation cascade and it is turned on by phosphorylation of its activation loop theme with the upstream kinases, Pbs2 (Brewster and rat style of diabetes by administration of streptozotocin in the current presence of SB239063.SB239063 attenuated diabetes-induced p38 phosphorylation and improved impairments in LV and endothelial function.Widder MRI assessment of ApoE?/? mouse aortas with AngII and SB239063.SB239063 inhibited p38 activity, irritation in atherosclerotic plaques and phagocytic activity of macrophages and reduced aortic main lesion size.Platelet activationAlrehani and aPL-induced monocyte adherence to HUVEC and respectively.LPS infusion enhanced p38 phosphorylation and TxA2 creation in platelets and leukocytes. SB203580 attenuated LPS-induced TxA2 discharge in platelets.Sakurai pig style of ischaemic preconditioning by LAD ligation (regional ischaemia).IP boosts co-localization of p38 with Cx43 and preserves phosphorylation of Cx43 during ischaemia. Inhibition of p38MAPK by SB203580 attenuated IP-induced IS-reduction and resulted in dephosphorylation of Cx43 that correlates using the propagation of I/R damage.Sanada canine style of ischaemic preconditioning by coronary occlusion (regional ischaemia).p38 MAPK activation during IP mainly mediates the cardioprotection accompanied by HSP27 phosphorylation/translocation. SB203580 treatment during IP blunted the infarct size restriction by IP and attenuated phosphorylation/translocation of HSP27.Marais et?al., 2001Langendorff-perfused rat hearts put through global ischaemia- reperfusion and cultured rat neonatal cardiac myocytesp38 was turned on during preconditioning and attenuated during following ischaemia. Non-preconditioned hearts acquired raised p38 activation compared. p38 inhibition by SB203580 during ischaemia and reperfusion is normally cardioprotective.Saurin et?al., 2000Ectopic appearance p38 or p38 isoforms in cultured rat neonatal cardiac myocytes put through simulated ischaemia in the current presence of SB203580.Inhibition of p38 during prolonged ischaemia reduced damage and contributed to preconditioning-induced cardioprotection.p38 and p38 differentially activated or deactivated respectively, during ischaemia.Nagarkatti et?al., 1998Simulated ischaemia in rat myoblast cell series H9c2.Inhibition of p38 prior to the starting point of SI blocks preconditioning, but is protective during prolonged ischaemia.Weinbrenner et?al., 1997Langendorff-perfused rabbit hearts put through global ischaemia-reperfusion in existence of SB203580Inhibition of p38 activation abolished security in preconditioned hearts and cardiomyocytes.Tong et?al., 2000Langendorff-perfused rat hearts, preconditioned with or without SB202190Preconditioning induced uptake of blood sugar was abrogated by the current presence of SB202190 Open up in another home window AEA, anandamide; ANF, atrial natriuretic peptide; AP, actions potentials; aPL, antiphospholipid antibodies; ApoE, apolipoprotein E; AngII, angiotensin II; bFGF, simple fibroblast growth aspect; CTGF, connective tissues growth aspect; Ctsk, cathepsin K; Cx43, distance junction proteins connexin43; DN, prominent harmful; FGF, fibroblast development aspect; GlcNAc, N-acetylglucosamine; H9c2, rat myoblast cell range; Hcy, homocysteine; HHcy, hyperhomocysteinaemia; ICAM, intercellular cell adhesion molecule; IP, ischaemic preconditioning; I/R, ischaemia/reperfusion; Is certainly, infarct size; ISO, isoproterenol; LAD, still left anterior descending coronary artery; LV, still left ventricle; MAPKAPK2, MAPK turned on PK 2; MI, myocardial infarction; MMP, matrix metalloproteinase; NADPH, nicotinamide adenine dinucleotide phosphate; NFAT, nuclear aspect of turned on T-cell; Npc1, NiemannCPick disease type C1; PCADK, poly(cyclohexane-1,4-diyl acetone dimethylene ketal); PE, phenylephrine; PEG-SOD, polyethylene glycol superoxide dismutase; PV, pulmonary vein; ROS, reactive air types; SB, SB203580; SERCA2, sarcoplasmic reticulum Ca2+ ATPase; SI, simulated ischaemia; SMA, simple muscle tissue actin; SMC, simple muscle tissue cell; TAC, transverse aortic constriction; TLR, Toll-like receptor; TxA2, thromboxane A2; WT, outrageous type. The results that p38 activation aggravates many the different parts of atherothrombosis and myocardial infarction, possess laid the building blocks for latest and relevant scientific trial activity. The firms with agencies under investigation consist of GlaxoSmithKline (losmapimod, different studies), ArrayBioPharma (ARRY-371797, “type”:”clinical-trial”,”attrs”:”text”:”NCT02057341″,”term_id”:”NCT02057341″NCT02057341) and Bristol-Myers Squibb (BMS-582949, “type”:”clinical-trial”,”attrs”:”text”:”NCT00570752″,”term_id”:”NCT00570752″NCT00570752), even though the latter programme appears inactive. GlaxoSmithKline gets the most energetic programme with several phase 1 studies recommending a potential advantage in sufferers with early (Cheriyan et?al., 2011) and past due (Sarov-Blat et?al., 2010; Elkhawad et?al., 2012) atherosclerosis. We’ve summarized.This study enrolled 535 patients with non-ST elevation myocardial infarction who had been randomized within a 3:3:2 ratio to oral losmapimod (two regimes, both of 7.5?mg daily with twice, or without, a 15?mg preliminary dosage) or placebo. signalling in center failing, where inhibition is effective inspite of the need for these human hormones to homeostasis. The issue is certainly whether equivalent benefits could accrue from p38 inhibition? Within this review, we will discuss the framework and function of p38, the annals of p38 inhibitors and their make use of in preclinical research. Finally, we will summarize the outcomes of latest cardiovascular clinical studies with p38 inhibitors. Dining tables of Links to become phosphorylated by and isoforms just (Cuenda (Parker homologue of p38 may be the pheromone and stress-sensing gene (Bell is certainly a component within a hierarchical activation cascade and it is turned on by phosphorylation of its activation loop theme with the upstream kinases, Pbs2 (Brewster and rat style of diabetes by administration of streptozotocin in the current presence of SB239063.SB239063 attenuated diabetes-induced p38 phosphorylation and improved impairments in LV and endothelial function.Widder MRI assessment of ApoE?/? mouse aortas with AngII and SB239063.SB239063 inhibited p38 activity, irritation in atherosclerotic plaques and phagocytic activity of macrophages and reduced aortic main lesion size.Platelet activationAlrehani and aPL-induced monocyte adherence to HUVEC and respectively.LPS infusion enhanced p38 phosphorylation and TxA2 creation in platelets and leukocytes. SB203580 attenuated LPS-induced TxA2 discharge in platelets.Sakurai pig style of ischaemic preconditioning by LAD ligation (regional ischaemia).IP boosts co-localization of p38 with Cx43 and preserves phosphorylation of Cx43 during ischaemia. Inhibition of p38MAPK by SB203580 attenuated IP-induced IS-reduction and resulted in dephosphorylation of Cx43 that correlates using the propagation of I/R damage.Sanada canine style of ischaemic preconditioning by coronary occlusion (regional ischaemia).p38 MAPK activation during IP mainly mediates the cardioprotection accompanied by HSP27 phosphorylation/translocation. SB203580 treatment during IP blunted the infarct size restriction by IP and attenuated phosphorylation/translocation of HSP27.Marais et?al., 2001Langendorff-perfused rat hearts put through global ischaemia- reperfusion and cultured rat neonatal cardiac myocytesp38 was turned on during preconditioning and attenuated during following ischaemia. Non-preconditioned hearts got raised p38 activation compared. p38 inhibition by SB203580 during ischaemia and reperfusion is certainly cardioprotective.Saurin et?al., 2000Ectopic appearance p38 or p38 isoforms in cultured rat neonatal cardiac myocytes put through simulated ischaemia in the current presence of SB203580.Inhibition of p38 during prolonged ischaemia reduced damage and contributed to preconditioning-induced cardioprotection.p38 and p38 differentially activated or deactivated respectively, during ischaemia.Nagarkatti et?al., 1998Simulated ischaemia in rat myoblast cell range H9c2.Inhibition of p38 prior to the starting point of SI blocks preconditioning, but is protective during prolonged ischaemia.Weinbrenner et?al., 1997Langendorff-perfused rabbit hearts put through global ischaemia-reperfusion in existence of SB203580Inhibition of p38 activation abolished security in preconditioned hearts and cardiomyocytes.Tong et?al., 2000Langendorff-perfused rat hearts, preconditioned with or without SB202190Preconditioning induced uptake of blood sugar was abrogated by the current presence of SB202190 Open up in another home window AEA, anandamide; ANF, atrial natriuretic peptide; AP, actions potentials; aPL, antiphospholipid antibodies; ApoE, apolipoprotein E; AngII, angiotensin II; bFGF, simple fibroblast growth aspect; CTGF, connective tissues growth aspect; Ctsk, cathepsin K; Cx43, distance junction proteins connexin43; DN, prominent harmful; FGF, fibroblast development aspect; GlcNAc, N-acetylglucosamine; H9c2, rat myoblast cell range; Hcy, homocysteine; HHcy, hyperhomocysteinaemia; ICAM, intercellular cell adhesion molecule; IP, ischaemic preconditioning; I/R, ischaemia/reperfusion; Is certainly, infarct size; ISO, isoproterenol; LAD, still left anterior descending coronary artery; LV, still left ventricle; MAPKAPK2, MAPK turned on PK 2; MI, myocardial infarction; MMP, matrix metalloproteinase; NADPH, nicotinamide adenine dinucleotide phosphate; NFAT, nuclear aspect of turned on T-cell; Npc1, NiemannCPick disease type C1; PCADK, poly(cyclohexane-1,4-diyl acetone dimethylene ketal); PE, phenylephrine; PEG-SOD, polyethylene glycol superoxide dismutase; PV, Nomilin pulmonary vein; ROS, reactive air types; SB, SB203580; SERCA2, sarcoplasmic reticulum Ca2+ ATPase; SI, simulated ischaemia; SMA, simple muscle tissue actin; SMC, simple muscle tissue cell; TAC, transverse aortic constriction; TLR, Toll-like receptor; TxA2, thromboxane A2; WT, outrageous type. The results that p38 activation aggravates many the different parts of atherothrombosis and myocardial infarction, possess laid the building blocks for latest and relevant scientific trial activity. The firms with agencies under investigation consist of GlaxoSmithKline (losmapimod, various trials), ArrayBioPharma (ARRY-371797, “type”:”clinical-trial”,”attrs”:”text”:”NCT02057341″,”term_id”:”NCT02057341″NCT02057341) and Bristol-Myers Squibb (BMS-582949, “type”:”clinical-trial”,”attrs”:”text”:”NCT00570752″,”term_id”:”NCT00570752″NCT00570752), although the latter programme seems.M. of these hormones to homeostasis. The question is whether similar benefits could accrue from p38 inhibition? In this review, we will discuss the structure and function of p38, the history of p38 inhibitors and their use in preclinical studies. Finally, we will summarize the results of recent cardiovascular clinical trials with p38 inhibitors. Tables of Links to be phosphorylated by and isoforms only (Cuenda (Parker homologue of p38 is the pheromone and stress-sensing gene (Bell is a component in a hierarchical activation cascade and is activated by phosphorylation of its activation loop motif by the upstream kinases, Pbs2 (Brewster and rat model of diabetes by administration of streptozotocin in the presence of SB239063.SB239063 attenuated diabetes-induced p38 phosphorylation and improved impairments in LV and endothelial function.Widder MRI assessment of ApoE?/? mouse aortas with AngII and SB239063.SB239063 inhibited p38 activity, inflammation in atherosclerotic plaques and phagocytic activity of macrophages and diminished aortic root lesion size.Platelet activationAlrehani and aPL-induced monocyte adherence to HUVEC and respectively.LPS infusion enhanced p38 phosphorylation and TxA2 production in platelets and leukocytes. SB203580 attenuated LPS-induced TxA2 release in platelets.Sakurai pig model of ischaemic preconditioning by LAD ligation (regional ischaemia).IP increases co-localization of p38 with Cx43 and preserves phosphorylation of Cx43 during ischaemia. Inhibition of p38MAPK by SB203580 attenuated IP-induced IS-reduction and led to dephosphorylation of Cx43 that correlates with the propagation of I/R injury.Sanada canine model of ischaemic preconditioning by coronary occlusion (regional ischaemia).p38 MAPK activation during IP mainly mediates the cardioprotection followed by HSP27 phosphorylation/translocation. SB203580 treatment during IP blunted the infarct size limitation by IP and attenuated phosphorylation/translocation of HSP27.Marais et?al., 2001Langendorff-perfused rat hearts subjected to global ischaemia- reperfusion and cultured rat neonatal cardiac myocytesp38 was activated during preconditioning and attenuated during subsequent ischaemia. Non-preconditioned hearts had elevated p38 activation in comparison. p38 inhibition by SB203580 during ischaemia and reperfusion is cardioprotective.Saurin et?al., 2000Ectopic expression p38 or p38 isoforms in cultured rat neonatal cardiac myocytes subjected to simulated ischaemia in the presence of SB203580.Inhibition of p38 during prolonged ischaemia reduced injury and contributed to preconditioning-induced cardioprotection.p38 and p38 differentially activated or deactivated respectively, during ischaemia.Nagarkatti et?al., 1998Simulated ischaemia in rat myoblast cell line H9c2.Inhibition of p38 before the onset of SI blocks preconditioning, but is protective during prolonged ischaemia.Weinbrenner et?al., 1997Langendorff-perfused rabbit hearts subjected to global ischaemia-reperfusion in presence of SB203580Inhibition of p38 activation abolished protection in preconditioned hearts and cardiomyocytes.Tong et?al., 2000Langendorff-perfused rat hearts, preconditioned with or without SB202190Preconditioning induced uptake of glucose was abrogated by the presence of SB202190 Rabbit polyclonal to Myocardin Open in a separate window AEA, anandamide; ANF, atrial natriuretic peptide; AP, action potentials; aPL, antiphospholipid antibodies; ApoE, apolipoprotein E; AngII, angiotensin II; bFGF, basic fibroblast growth factor; CTGF, connective tissue growth factor; Ctsk, cathepsin K; Cx43, gap junction protein connexin43; DN, dominant negative; FGF, fibroblast growth factor; GlcNAc, N-acetylglucosamine; H9c2, rat myoblast cell line; Hcy, homocysteine; HHcy, hyperhomocysteinaemia; ICAM, intercellular cell adhesion molecule; IP, ischaemic preconditioning; I/R, ischaemia/reperfusion; IS, infarct size; ISO, isoproterenol; LAD, left anterior descending coronary artery; LV, left ventricle; MAPKAPK2, MAPK activated PK 2; MI, myocardial infarction; MMP, matrix metalloproteinase; NADPH, nicotinamide adenine dinucleotide phosphate; NFAT, nuclear factor of activated T-cell; Npc1, NiemannCPick disease type C1; PCADK, poly(cyclohexane-1,4-diyl acetone dimethylene ketal); PE, phenylephrine; PEG-SOD, polyethylene glycol superoxide dismutase; PV, pulmonary vein; ROS, reactive oxygen.