ライフサイエンスコーパス: lipotoxic

1 ival, it was not nephrotoxic, myelotoxic, or lipotoxic and did not increase CsA-induced nephrotoxicit

2 hinese hamster ovary cell lines resistant to lipotoxic and oxidative stress.

3 ytoplasm by a mechanism that is regulated by lipotoxic and oxidative stress.

4 drial metabolic sink whereby accumulation of lipotoxic byproducts leads to lipoapoptosis, loss of car

5 in flies and identifies a potential link to lipotoxic cardiac diseases in humans.

6 ietary SFAs in the molecular pathogenesis of lipotoxic cardiomyopathy and hypertrophy.

7 s a potential therapeutic target in treating lipotoxic cardiomyopathy and other heart diseases.

8 on of eEF1A-1 expression in a mouse model of lipotoxic cardiomyopathy implicate this cellular respons

9 hat CD36 is necessary for the development of lipotoxic cardiomyopathy in MHC-PPARalpha mice and that

10 While the primary etiology of lipotoxic cardiomyopathy is an elevation of lipid levels

11 Dilated lipotoxic cardiomyopathy is the consequence of excess li

12 In 2000, a syndrome of "lipotoxic cardiomyopathy" resembling earlier pathologic

13 To test this hypothesis, mice with severe lipotoxic cardiomyopathy, induced transgenically by card

14 l mechanism for mitochondrial dysfunction in lipotoxic cardiomyopathy.

15 ion, bioenergetics, and premature death with lipotoxic cardiomyopathy.

16 ia the MHC promoter (MHC-ACS), which develop lipotoxic cardiomyopathy.

17 a form of cardiac dysfunction referred to as lipotoxic cardiomyopathy.

18 ic myocardial PPAR-delta deficiency leads to lipotoxic cardiomyopathy.

19 models, PPARgamma agonist treatment improves lipotoxic cardiomyopathy; however, PPARgamma agonist tre

20 palmitate, suggesting that eEF1A-1 mediates lipotoxic cell death, secondary to oxidative and ER stre

21 e cytosol and serve as critical mediators of lipotoxic cell death.

22 e, an enzyme involved in the biosynthesis of lipotoxic ceramides that antagonize insulin action.

23 adipose tissues of obese rodents may lead to lipotoxic complications such as diabetes.

24 red out of 673 detected, p < 0.05) confirmed lipotoxic conditions and oxidative stress by showing an

25 e mechanistic consequences of glucotoxic and lipotoxic conditions on human islets in vivo and develop

26 bioactive lipid intermediates, formed under lipotoxic conditions, are involved in these processes.

27 Under lipotoxic conditions, palmitate inhibits hepatic macroph

28 ant from this screen demonstrated that under lipotoxic conditions, small nucleolar RNAs (snoRNAs) in

29 tic insulin resistance, despite the apparent lipotoxic conditions.

30 letal muscle and pancreatic beta-cells under lipotoxic conditions.

31 lation of inactivated fatty acids results in lipotoxic damage and increased steatosis.

32 aperone results in marked protection against lipotoxic death in macrophages and prevents macrophage f

33 tive leptin action as the proximate cause of lipotoxic diabetes in ZDF rats.

34 Thus far, lipotoxic diabetes of fa/fa Zucker diabetic fatty rats i

35 degenerative disease, but the possibility of lipotoxic disease of skeletal and/or cardiac muscle may

36 lts implicate ARV1 as a protective factor in lipotoxic diseases due to modulation of fatty acid metab

37 ic steatohepatitis (NASH) is an inflammatory lipotoxic disorder, but how inflammatory cells are recru

38 trategies to avert the predicted epidemic of lipotoxic disorders.

39 on to prevent acylcarnitine accumulation and lipotoxic dysregulation of mitochondria.

40 i-oxidant MCI-186 significantly reversed the lipotoxic effect by decreasing the generation of ROS and

41 stance, suggests that excess FFA may exert a lipotoxic effect on the heart.

42 nfirmed cell death through apoptosis and the lipotoxic effect was more dramatic in SC cultures grown

43 e tissue can be cardioprotective by reducing lipotoxic effects in other peripheral tissues and by mai

44 oplasmic reticulum stress and the UPR in the lipotoxic effects of Mttp deletion, we administered taur

45 ects of cardiometabolic disorders, including lipotoxic endoplasmic reticulum stress in macrophages.

46 This study elucidates the crosstalk between lipotoxic ER stress and the mitochondrial pathway of apo

47 , but only the latter was causally linked to lipotoxic ER stress.

48 rage exceeds intracellular needs and induces lipotoxic events, ultimately contributing to the develop

49 y of skeletal muscle, potentially preventing lipotoxic FA accumulation, the dominant cause of insulin

50 asome in response to urate crystals, ATP and lipotoxic fatty acids.

51 A transporter CD36 in the pathophysiology of lipotoxic forms of cardiomyopathy.

52 ither intramyocardial lipid accumulation nor lipotoxic hallmarks were detected in SKO mice.

53 ailability results in lipid accumulation and lipotoxic heart disease.

54 f mouse bone-marrow-derived macrophages with lipotoxic hepatocyte-derived EVs induced macrophage chem

55 We previously reported that lipotoxic hepatocytes release CXCL10-enriched extracellu

56 L10)-laden extracellular vesicles (EVs) from lipotoxic hepatocytes, which induce macrophage chemotaxi

57 ectrum of wound-healing responses induced by lipotoxic hepatocytes.

58 mechanisms underlying the activation of this lipotoxic inflammasome.

59 ency-induced diabetes, and palmitate-induced lipotoxic insults in muscle and pancreatic beta-cells.

60 pid overstorage in cardiac myocytes produces lipotoxic intermediates that cause apoptosis, which lead

61 sis that impaired FAO causes accumulation of lipotoxic intermediates that inhibit muscle insulin sign

62 , that in concert promote the development of lipotoxic liver disease, a term that more accurately des

63 The lipotoxic liver injury hypothesis for the pathogenesis o

64 cornerstones of treatment and prevention of lipotoxic liver injury, a disease hitherto called NASH.

65 esponses among individuals determine whether lipotoxic livers regenerate, leading to stabilization or

66 nce by depleting CD4+ T helper cells through lipotoxic mechanisms associated with NAFLD.

67 ndrome." In conclusion, these data support a lipotoxic model of FFA-mediated lysosomal destabilizatio

68 age-specific manifestation of a more general lipotoxic pathogenic mechanism.

69 g and oxidation would be associated with the lipotoxic phenotype.

70 This occurred in parallel with a reduced lipotoxic pressure in skeletal muscle due to an upregula

71 rafficking and ER stress, partially reversed lipotoxic reductions in ER sphingomyelin (SM) content an

72 of ceramide synthesis, is important for the lipotoxic response and may contribute to the pathogenesi

73 Cellular mechanisms involved in the lipotoxic response will be discussed.

74 e several novel strategies to counteract the lipotoxic signaling of PA.

75 lasmic reticulum (ER) stress when exposed to lipotoxic signals associated with atherosclerosis, altho

76 daptive metabolic alterations underlying the lipotoxic state.

77 ly regulated and function to protect EC from lipotoxic stress and provide FA for metabolic needs.

78 Here we report that gadd7 is induced by lipotoxic stress in a reactive oxygen species (ROS)-depe

79 Moreover, LD formation protects EC from lipotoxic stress, regulates EC glycolysis, and provides

80 y shown to promote beta-cell survival during lipotoxic stress.

81 syndrome may be the human equivalent of the lipotoxic syndrome of rodents.