Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently shown improved survival following intestinal ischemia-reperfusion in a model that utilized aggressive crystalloid resuscitation sufficient to eliminate reperfusion-induced cardiovascular instability. The aims of this study were to determine whether the salutary effects associated with this regimen were due to: 1) prevention of systemic metabolic derangements; 2) attenuation of secondary organ injury; or 3) modulation of the systemic immune response. Under anesthesia, 4-week-old (65-85 g) male Sprague-Dawley rats (N = 63) received crystalloids at either 15 or 65 ml.kg-1.h-1 intravenously and were subjected to 90 min of superior mesenteric artery occlusion followed by 90 min of reperfusion (IR15, IR65) or time-matched sham (SH) operation (SH15, SH65). Results indicate that inadequate fluid resuscitation following intestinal IR was associated with significant serum hyperkalemia and hyperphosphatemia, acute renal insufficiency, and enhanced serum interleukin-6 levels. Maintenance of cardiovascular stability with aggressive fluid resuscitation was associated with an attenuation of these alterations. Therefore, the prevention of circulatory shock and the attenuation of distant organ injury and inflammatory response are associated with improved survival when an aggressive crystalloid resuscitation regimen is applied after intestinal ischemiareperfusion in immature rats.
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PMID:Aggressive fluid resuscitation following intestinal ischemia-reperfusion in immature rats prevents metabolic derangements and down regulates interleukin-6 release. 774 42

A 24-year-old black man presented with diffuse musculoskeletal pain and shotty lymphadenopathy. Laboratory studies revealed hypercalcemia and hyperphosphatemia, very high serum alkaline phosphatase activity, diffuse but intense uptake of radionuclide on a bone scan, urinary N-telopeptide excretion 30 times the upper limit of normal, and serum interleukin-6 100 times the upper limit of normal. An extensive workup for etiologies of the disorder was negative. A bone biopsy revealed intense osteoclastic resorption coupled with rapid bone formation and/or remodeling. This case appears to represent a new entity. Treatment with bisphosphonates produced symptomatic and biochemical improvement.
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PMID:Rapid skeletal turnover and hypercalcemia associated with markedly elevated interleukin-6 levels in a young black man. 951 22

Phosphate binders are useful for the treatment of hyperphosphatemia in hemodialysis (HD) patients. This study was performed to examine the effects of switching from calcium carbonate (CC) to lanthanum carbonate (LC) on bone mineral metabolism and inflammatory markers in HD patients. We conducted 29 stable HD patients receiving CC, which was replaced by LC and followed-up for 12 weeks. Patients underwent determinants of blood chemistries such as serum calcium (Ca), phosphorus, parathyroid hormone (PTH) and vitamin D status, and interleukin-6 (IL-6) mRNA levels in whole blood cells were evaluated by real-time PCR just before and after the treatment with LC. Corrected Ca [corrected] levels were significantly reduced, but serum phosphorus levels (P levels) were unchanged after LC treatment. Switching to LC increased whole-PTH, osteocalcin, 1,25(OH)(2) D(3) levels and 1,25(OH)(2) D(3)/25(OH)D(3) ratio. 1,25(OH)(2) D(3)/25(OH)D(3) ratio was negatively correlated with HD duration. Furthermore, whole blood cell IL-6 mRNA levels were significantly reduced by LC treatment. We provided that the switching from CC to LC improved Ca overload and ameliorated vitamin D and inflammatory status in HD patients. These observations suggest that LC may play a protective role for the progression of atherosclerosis and vascular calcification in these patients.
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PMID:Effects of switching from calcium carbonate to lanthanum carbonate on bone mineral metabolism in hemodialysis patients. 2358 11

Excessive phosphorus intake causes diseases such as hyperphosphatemia and hypocalcaemia, but the effect of dietary insufficiency of phosphorus is unclear. Here, we explored the effect of phosphorus dietary insufficiency on tissue growth and maintenance by using C57BL/6J mice fed a low phosphorus diet, which contained 18.5% of the phosphorus of a normal diet. We demonstrated that the phosphorus content in the maternal milk of mother mice was significantly reduced due to the consumption of a low phosphorus diet, which further resulted in bone deformation in infant mice in a female-specific manner. Polarizing microscopic analysis of low-phosphorus milk (LPM)-induced bone deformation resulted in unusually formed crystals inside cartilage. Furthermore, immunohistochemical analysis revealed ectopic expression of collagen I in the region where crystals were ectopically formed. Electron microscopic analysis showed morphological features similar to bone tissues. Immunochemical analysis demonstrated that the amount of interleukin-6 (IL-6), a cytokine known to trigger osteoclast formation, was significantly reduced in the maternal milk of mice fed the low-phosphorus diet. Our results suggest that phosphorus intake from maternal milk is involved in infant cartilage formation.
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PMID:Phosphorus-insufficient maternal milk is associated with ectopic expression of collagen I and female-specific bony changes in infant mouse cartilages. 3124 36

Cardiovascular calcification is associated with cardiovascular morbidity and mortality of patients with end-stage renal diseases (ESRD). Hyperphosphatemia and many of the inflammatory markers and mediators, including interleukin-6 (IL-6), are considered as the major risk factors of cardiovascular calcification. Although cellular senescence may be involved in cardiovascular calcification caused by phosphate overload and (or) IL-6 in patients with ESRD, less is known about the underlying mechanisms for phosphate- and IL-6-induced senescence-associated calcification of vascular smooth muscle cells (VSMCs). In the present study, we investigated the correlation between cellular senescence and vascular calcification induced by loading phosphate and (or) IL-6 in VSMCs. Our findings show that p53 plays a major role in senescence-associated vascular calcification induced by phosphate overload. IL-6 induces senescence-associated calcification in VSMCs depending upon activation of the IL-6/soluble IL-6 receptor (sIL-6R)/signal transducer and activator of transcription 3 (STAT3)/p53/p21 pathway. We demonstrate that the synergistic action of phosphate overload and IL-6 enhances senescence-associated calcification in a p53-dependent manner and is inhibited by an anti-aging agent (resveratrol) in a dose-dependent manner.
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PMID:The synergistic action of phosphate and interleukin-6 enhances senescence-associated calcification in vascular smooth muscle cells depending on p53. 3137 99