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1 idic devices, injured on-chip by exposure to lipotoxic agent (palmitate), and then connected to the b
2                         DAGs are known to be lipotoxic and associated with atherosclerosis.
3 ival, it was not nephrotoxic, myelotoxic, or lipotoxic and did not increase CsA-induced nephrotoxicit
4 he capacity for storage and oxidation can be lipotoxic and induce non-ischaemic and non-hypertensive
5 ytoplasm by a mechanism that is regulated by lipotoxic and oxidative stress.
6 hinese hamster ovary cell lines resistant to lipotoxic and oxidative stress.
7                                              Lipotoxic and proteotoxic stress can activate the unfold
8 drial metabolic sink whereby accumulation of lipotoxic byproducts leads to lipoapoptosis, loss of car
9  in flies and identifies a potential link to lipotoxic cardiac diseases in humans.
10 ietary SFAs in the molecular pathogenesis of lipotoxic cardiomyopathy and hypertrophy.
11 s a potential therapeutic target in treating lipotoxic cardiomyopathy and other heart diseases.
12 e find that intergenerational inheritance of lipotoxic cardiomyopathy correlates with elevated system
13 on of eEF1A-1 expression in a mouse model of lipotoxic cardiomyopathy implicate this cellular respons
14 hat CD36 is necessary for the development of lipotoxic cardiomyopathy in MHC-PPARalpha mice and that
15                While the primary etiology of lipotoxic cardiomyopathy is an elevation of lipid levels
16                                      Dilated lipotoxic cardiomyopathy is the consequence of excess li
17                      In 2000, a syndrome of "lipotoxic cardiomyopathy" resembling earlier pathologic
18          Obesity is strongly correlated with lipotoxic cardiomyopathy, heart failure and thus mortali
19    To test this hypothesis, mice with severe lipotoxic cardiomyopathy, induced transgenically by card
20 nal status may predispose their offspring to lipotoxic cardiomyopathy.
21 l mechanism for mitochondrial dysfunction in lipotoxic cardiomyopathy.
22 ertensive cardiomyopathy, termed diabetic or lipotoxic cardiomyopathy.
23 ion, bioenergetics, and premature death with lipotoxic cardiomyopathy.
24 ia the MHC promoter (MHC-ACS), which develop lipotoxic cardiomyopathy.
25 a form of cardiac dysfunction referred to as lipotoxic cardiomyopathy.
26 ic myocardial PPAR-delta deficiency leads to lipotoxic cardiomyopathy.
27 models, PPARgamma agonist treatment improves lipotoxic cardiomyopathy; however, PPARgamma agonist tre
28  palmitate, suggesting that eEF1A-1 mediates lipotoxic cell death, secondary to oxidative and ER stre
29 e cytosol and serve as critical mediators of lipotoxic cell death.
30 ved cells are hypersensitive to SFA-mediated lipotoxic cell death.
31 vivo and aqueous media, resulting in greater lipotoxic cellular responses and organ failure.
32 e, an enzyme involved in the biosynthesis of lipotoxic ceramides that antagonize insulin action.
33 adipose tissues of obese rodents may lead to lipotoxic complications such as diabetes.
34                                        Under lipotoxic condition, the effects of p66Shc are mediated
35 red out of 673 detected, p < 0.05) confirmed lipotoxic conditions and oxidative stress by showing an
36 s downstream of lysosomal alkalization under lipotoxic conditions and that recovery of lysosomal acid
37 -cell insulin resistance that develops under lipotoxic conditions and with excess body fat.
38 lar mechanism for the defective autophagy in lipotoxic conditions is not fully known.
39 e mechanistic consequences of glucotoxic and lipotoxic conditions on human islets in vivo and develop
40  bioactive lipid intermediates, formed under lipotoxic conditions, are involved in these processes.
41                                        Under lipotoxic conditions, palmitate inhibits hepatic macroph
42 ant from this screen demonstrated that under lipotoxic conditions, small nucleolar RNAs (snoRNAs) in
43 y step during the repression of autophagy in lipotoxic conditions.
44 letal muscle and pancreatic beta-cells under lipotoxic conditions.
45 tic insulin resistance, despite the apparent lipotoxic conditions.
46 lation of inactivated fatty acids results in lipotoxic damage and increased steatosis.
47 aperone results in marked protection against lipotoxic death in macrophages and prevents macrophage f
48 tive leptin action as the proximate cause of lipotoxic diabetes in ZDF rats.
49                                    Thus far, lipotoxic diabetes of fa/fa Zucker diabetic fatty rats i
50 iabetes onset, driven by the accumulation of lipotoxic diacylglycerols and ceramides, alongside a red
51 degenerative disease, but the possibility of lipotoxic disease of skeletal and/or cardiac muscle may
52 lts implicate ARV1 as a protective factor in lipotoxic diseases due to modulation of fatty acid metab
53 f the pathophysiology of hyperlipidemia, and lipotoxic diseases such as some forms of cardiomyopathy
54 ic steatohepatitis (NASH) is an inflammatory lipotoxic disorder, but how inflammatory cells are recru
55 trategies to avert the predicted epidemic of lipotoxic disorders.
56 ssues not suited for fat storage, leading to lipotoxic disruption of cell function and survival.
57 on to prevent acylcarnitine accumulation and lipotoxic dysregulation of mitochondria.
58 i-oxidant MCI-186 significantly reversed the lipotoxic effect by decreasing the generation of ROS and
59 stance, suggests that excess FFA may exert a lipotoxic effect on the heart.
60 nfirmed cell death through apoptosis and the lipotoxic effect was more dramatic in SC cultures grown
61  although high-level PA (HPA) indeed induces lipotoxic effects in liver cells, low-level PA (LPA) inc
62 e tissue can be cardioprotective by reducing lipotoxic effects in other peripheral tissues and by mai
63 oplasmic reticulum stress and the UPR in the lipotoxic effects of Mttp deletion, we administered taur
64 nsaminase activity significantly reduced the lipotoxic effects of palmitate, whereas knockdown of glu
65 ects of cardiometabolic disorders, including lipotoxic endoplasmic reticulum stress in macrophages.
66                               This creates a lipotoxic environment, impairing placental efficiency.
67                        This review discusses lipotoxic ER stress and the central role of the ER in co
68  This study elucidates the crosstalk between lipotoxic ER stress and the mitochondrial pathway of apo
69 , but only the latter was causally linked to lipotoxic ER stress.
70 rage exceeds intracellular needs and induces lipotoxic events, ultimately contributing to the develop
71 y of skeletal muscle, potentially preventing lipotoxic FA accumulation, the dominant cause of insulin
72                                              Lipotoxic factors and insulin resistance were evaluated
73                                 Accordingly, lipotoxic factors were increased in DM versus non-DM rec
74 tly, metformin use was associated with fewer lipotoxic factors.
75 asome in response to urate crystals, ATP and lipotoxic fatty acids.
76 A transporter CD36 in the pathophysiology of lipotoxic forms of cardiomyopathy.
77 ither intramyocardial lipid accumulation nor lipotoxic hallmarks were detected in SKO mice.
78 ailability results in lipid accumulation and lipotoxic heart disease.
79 f mouse bone-marrow-derived macrophages with lipotoxic hepatocyte-derived EVs induced macrophage chem
80               Neutrophil infiltration around lipotoxic hepatocytes is a hallmark of nonalcoholic stea
81                  We previously reported that lipotoxic hepatocytes release CXCL10-enriched extracellu
82 L10)-laden extracellular vesicles (EVs) from lipotoxic hepatocytes, which induce macrophage chemotaxi
83 ectrum of wound-healing responses induced by lipotoxic hepatocytes.
84 mechanisms underlying the activation of this lipotoxic inflammasome.
85 indings highlight Cer as early indicators of lipotoxic injury and support Sita's potential for CMD th
86 e lipolysis make CEL an unlikely mediator of lipotoxic injury in AP.
87 P2 were equipotent in inducing lipolysis and lipotoxic injury, CEL required bile acid concentrations
88  renal cell line (HEK 293) was used to study lipotoxic injury.
89 tic transcriptomic landscapes in response to lipotoxic insults across multiple species.
90 ency-induced diabetes, and palmitate-induced lipotoxic insults in muscle and pancreatic beta-cells.
91 nflammatory onset, prevented accumulation of lipotoxic intermediates (ceramides and diacylglycerols)
92 pid overstorage in cardiac myocytes produces lipotoxic intermediates that cause apoptosis, which lead
93 sis that impaired FAO causes accumulation of lipotoxic intermediates that inhibit muscle insulin sign
94 H4IIEC3 rat hepatoma cells were treated with lipotoxic levels of palmitate while modulating anaplerot
95 in particle composition and size and reduced lipotoxic lipid species.
96 , that in concert promote the development of lipotoxic liver disease, a term that more accurately des
97                                          The lipotoxic liver injury hypothesis for the pathogenesis o
98  cornerstones of treatment and prevention of lipotoxic liver injury, a disease hitherto called NASH.
99 gs targeting energy intake, energy disposal, lipotoxic liver injury, and the resulting inflammation a
100 esponses among individuals determine whether lipotoxic livers regenerate, leading to stabilization or
101 ooxyacetic acid confirmed that reductions in lipotoxic markers were associated with decreases in anap
102 nce by depleting CD4+ T helper cells through lipotoxic mechanisms associated with NAFLD.
103 eu (hyperglycemia and insulin resistance) on lipotoxic-mediated injury.
104 r lipid exchange and disposal of potentially lipotoxic metabolites, producing distinct lipid distribu
105 ndrome." In conclusion, these data support a lipotoxic model of FFA-mediated lysosomal destabilizatio
106 ken together, these results demonstrate that lipotoxic palmitate treatments enhance anaplerosis in cu
107 age-specific manifestation of a more general lipotoxic pathogenic mechanism.
108 ther, these data indicate that activation of lipotoxic pathways are the result of space stressors alo
109 g and oxidation would be associated with the lipotoxic phenotype.
110     This occurred in parallel with a reduced lipotoxic pressure in skeletal muscle due to an upregula
111 rafficking and ER stress, partially reversed lipotoxic reductions in ER sphingomyelin (SM) content an
112  of ceramide synthesis, is important for the lipotoxic response and may contribute to the pathogenesi
113          Cellular mechanisms involved in the lipotoxic response will be discussed.
114 e several novel strategies to counteract the lipotoxic signaling of PA.
115 lasmic reticulum (ER) stress when exposed to lipotoxic signals associated with atherosclerosis, altho
116 daptive metabolic alterations underlying the lipotoxic state.
117 ly regulated and function to protect EC from lipotoxic stress and provide FA for metabolic needs.
118 ocytes seems to be a key mechanism to combat lipotoxic stress by shunting out miR-122 from stressed h
119                                  In summary, lipotoxic stress enhances the expression of LSEC VCAM-1,
120      Here we report that gadd7 is induced by lipotoxic stress in a reactive oxygen species (ROS)-depe
121      Moreover, LD formation protects EC from lipotoxic stress, regulates EC glycolysis, and provides
122 y improves NASH and fibrosis despite ongoing lipotoxic stress.
123 embrane lipid homeostasis and prevents acute lipotoxic stress.
124 y shown to promote beta-cell survival during lipotoxic stress.
125  syndrome may be the human equivalent of the lipotoxic syndrome of rodents.
126 rating a strong potential for advancing this lipotoxic treatment strategy to clinical application.
127                     Because free FAs are key lipotoxic triggers accelerating disease progression, inh

 
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