Pro-inflammatory states and IGF-I level in ischemic heart disease with low or high serum iron

Lee, Shin-Da; Huang, Chih Yang; Shu, Wen; Chen, Ter Hsin; Lin, James A.; Hsu, Hsi Hsien; Lin, Chung-Saint; Liu, Chung‐Jung; Kuo, Wei Wen; Chen, Li Mien

doi:10.1016/j.cca.2006.01.012

Cited by 19 publications

(10 citation statements)

References 26 publications

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“…Eccentric cardiac hypertrophy, in which chamber volume enlarges without a relative increase or even with a relative decrease in its wall thickness, is known to progress to dilated cardiomyopathy, heart failure and sudden death (Rossi & Carillo, 1991; Nicol et al 2001). Accumulating evidence indicates that pro‐inflammatory cytokines and growth factors play pathogenic roles in myocardial remodelling processes, including cardiac hypertrophy and apoptosis, in various cardiac diseases (Neyses & Pelzer, 1995; Hirano, 1998; Lee et al 2006 a , c ). Tumour necrosis factor‐α (TNFα) and insulin‐like growth factor (IGF)‐II have also been implicated in the pathophysiology of cardiac hypertrophy (Lee et al 2006 b ).…”

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confidence: 99%

Eccentric cardiac hypertrophy was induced by long‐term intermittent hypoxia in rats

Chen

Kuo

Yang

et al. 2007

Experimental Physiology

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It is unclear whether cardiac hypertrophy and hypertrophy-related pathways will be induced by long-term intermittent hypoxia. Thirty-six Sprague-Dawley rats were randomly assigned into three groups: normoxia, and long-term intermittent hypoxia (12% O 2 , 8 h per day) for 4 weeks (4WLTIH) or for 8 weeks (8WLTIH). Myocardial morphology, trophic factors and signalling pathways in the three groups were determined by heart weight index, histological analysis, Western blotting and reverse transcriptase-polymerase chain reaction from the excised left ventricle. The ratio of whole heart weight to body weight, the ratio of left ventricular weight to body weight, the gross vertical cross-section of the heart and myocardial morphological changes were increased in the 4WLTIH group and were further augmented in the 8WLTIH group. In the 4WLTIH group, tumour necrosis factor-α(TNFα), insulin-like growth factor (IGF)-II, phosphorylated p38 mitogen-activated protein kinase (P38), signal transducers and activators of transcription (STAT)-1 and STAT-3 were significantly increased in the cardiac tissues. However, in the 8WLTIH group, in addition to the above factors, interleukin-6, mitogen-activated protein kinase (MEK)5 and extracellular signal-regulated kinase (ERK)5 were significantly increased compared with the normoxia group. We conclude that cardiac hypertrophy associated with TNFα and IGF-II was induced by intermittent hypoxia. The longer duration of intermittent hypoxia further activated the eccentric hypertrophy-related pathway, as well as the interleukin 6-related MEK5-ERK5 and STAT-3 pathways, which could result in the development of cardiac dilatation and pathology.

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confidence: 99%

Eccentric cardiac hypertrophy was induced by long‐term intermittent hypoxia in rats

Chen

Kuo

Yang

et al. 2007

Experimental Physiology

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“…In HD patients, increased ferritin levels reflect a decrease in iron‐specific antioxidant activity and represents a risk factor for advanced cardiovascular damage 27 . Our previous study also show that higher cardiovascular risks are associated with elevated serum ferritin in IHD patients 9 . Also, low TIBC is a risk factor for cardiovascular diseases 11 .…”

Section: Discussionmentioning

confidence: 82%

“…Our previous study showed that IHD patients with lower serum iron have a higher cardiovascular risk than IHD patients with normal serum iron. 9 Increased serum ferritin has been associated with cardiovascular mortality and was also suggested as an independent predictor of cardiovascular mortality. 10,27 In HD patients, increased ferritin levels reflect a decrease in iron-specific antioxidant activity and represents a risk factor for advanced cardiovascular damage.…”

Section: Discussionmentioning

confidence: 99%

“…8 Low serum irons (SI) were associated with less cardiac protection and more proinflammatory states in patients with ischaemic heart diseases (IHD) than normal subjects. 9 Increased serum ferritin was suggested as an independent predictor of cardiovascular mortality. 10 Lower total iron-binding capacity (TIBC), is an independent negative risk factor for cardiovascular diseases, which suggest that lower TIBC is a higher risk factor for cardiovascular diseases.…”

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Iron status and cardiovascular risk factors in patients with haemodialysis versus patients with ischaemic heart disease

Cheng

Kuo

et al. 2009

Nephrology

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Imbalanced iron status in patients on HD coexisted with abnormal lipid profiles, increased anaerobic activity and higher inflammatory status, which suggests that imbalanced iron status in HD patients may play a deleterious role in cardiovascular pathophysiology. Altered GH-IGF axis found in HD patients was more obvious than in IHD patients. This may imply that the GH-IGF axis system is modulated or adapted by HD.

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“…Blockade of inflammatory cytokines has been shown to be effective in preventing the alteration in sepsis-induced IGF levels [16, 18], suggesting inflammatory cytokines can repress this important protein synthesis signaling pathway. In addition, increased levels of inflammatory cytokines, concomitant with decreased activity of the IGF system, have been observed in aging [20], chronic inflammation [20], inflammatory bowel disease [21], and ischemic heart disease [22], conditions also associated with muscle protein loss. In addition, pro-inflammatory cytokines have also been shown to promote protein degradation [23].…”

Section: Introductionmentioning

confidence: 99%

Induction of muscle weakness by local inflammation: an experimental animal model

et al. 2009

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Objective and design-The objective of this study was to characterize the response of skeletal muscle to a localized inflammation induced by the inflammatory agent casein.Methods-An inflammatory agent, casein, was injected into the right hindlimb and saline was injected into the left hindlimb of normal adult mice, once daily for six consecutive days. Inflammatory response was monitored by immunohistochemical labeling of leukocytes. Muscle protein levels were determined by electrophoresis and muscle function was determined by isometric force measurements.Results-Local inflammation was induced by casein in association with the accumulation of extensive neutrophils and macrophages in the solues muscle. This local inflammation resulted in a shift in myosin heavy chain (MHC) isoform expression and a significant reduction in total MHC concentration in the soleus. Maximal twitch and tetanic forces were significantly reduced in the inflamed soleus. Contractile function in soleus was fully restored after two weeks of recovery, along with the restoration of protein concentration and the disappearance of inflammatory cells.Conclusion-This study establishes a unique and robust model in which mechanisms of local inflammation induced muscle protein degradation, reduction of contractile force, and subsequent recovery from this condition can be further studied.

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Pro-inflammatory states and IGF-I level in ischemic heart disease with low or high serum iron

Cited by 19 publications

References 26 publications

Eccentric cardiac hypertrophy was induced by long‐term intermittent hypoxia in rats

Eccentric cardiac hypertrophy was induced by long‐term intermittent hypoxia in rats

Iron status and cardiovascular risk factors in patients with haemodialysis versus patients with ischaemic heart disease

Induction of muscle weakness by local inflammation: an experimental animal model

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