Skeletal muscle wastage in Crohn's disease: A pathway shared with heart failure?

Cuoco, L.; Vescovo, Giorgio; Castaman, R.; Ravara, Barbara; Cammarota, Giovanni; Angelini, Annalisa; Salvagnini, M.; Libera, Luciano Dalla

doi:10.1016/j.ijcard.2007.06.006

Cited by 34 publications

(73 citation statements)

References 55 publications

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“…26,28 It was recently reported that CD patients had muscle atrophy, with a reduced muscle fiber size, increased apoptosis, and a shift of myosin heavy chains from the slow to the fast type. 29 Yet FFM and FM in the whole CD cohort were not significantly different from controls. This is consistent with the fact that muscle mass only accounts for 50% of lean mass, and explains why FFM is not a sensitive measure.…”

Section: Discussionmentioning

confidence: 78%

Sarcopenia is prevalent in patients with Crohnʼs disease in clinical remission

Schneider

Al-Jaouni

Filippi

et al. 2008

Inflammatory Bowel Diseases

125

133

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Section: Discussionmentioning

confidence: 78%

Sarcopenia is prevalent in patients with Crohnʼs disease in clinical remission

Schneider

Al-Jaouni

Filippi

et al. 2008

Inflammatory Bowel Diseases

125

133

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“…Heart and kidney samples were homogenized and solubilized in sodium dodecyl sulfate (SDS) buffer [9,15]. Protein quantification was performed using the Qubit® Protein Assay Kit (Life Technologies) according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

“…A high venous pressure is an alternative and important cause of worsening kidney function; in this case, tubular damage plays a major role [6] and simultaneously constitutes a stimulus for peripheral synthesis and the release of inflammatory mediators [7]. Moreover, inflammation could be an additional nonhemodynamic mechanism for the progression of chronic kidney disease [5,8] triggered by local kidney factors or by increased gut absorption of endotoxin [9,10]. In fact, patients with severe HF feature high levels of tumor necrosis factor (TNF)-α and interleukins (IL) [11].…”

Section: Introductionmentioning

confidence: 99%

The Role of Congestion in Cardiorenal Syndrome Type 2: New Pathophysiological Insights into an Experimental Model of Heart Failure

et al. 2015

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Background: In cardiorenal syndrome type 2 (CRS2), the role of systemic congestion in heart failure (HF) is still obscure. We studied a model of CRS2 [monocrotaline (MCT)-treated rats] secondary to pulmonary hypertension and right ventricular (RV) failure in order to evaluate the contribution of prevalent congestion to the development of kidney injury. Methods: Ten animals were treated with MCT for 4 weeks until they developed HF. Eleven animals were taken as controls. Signs of hypertrophy and dilatation of the right ventricle demonstrated the occurrence of HF. Brain natriuretic peptide (BNP), serum creatinine (sCreatinine), both kidney and heart neutrophil gelatinase-associated lipocalin (NGAL), matrix metallopeptidase 9 (MMP9), serum cytokines as well as kidney and heart cell death, as assessed by TUNEL, were studied. Results: Rats with HF showed higher BNP levels [chronic HF (CHF) 4.8 ± 0.5 ng/ml; controls 1.5 ± 0.2 ng/ml; p < 0.0001], marked RV hypertrophy and dilatation (RV mass/RV volume: CHF 1.46 ± 0.31, controls 2.41 ± 0.81; p < 0.01) as well as pleural and peritoneal effusions. A significant increase in proinflammatory cytokines and sCreatinine was observed (CHF 3.06 ± 1.3 pg/ml vs. controls 0.54 ± 0.23 pg/ml; p = 0.04). Serum (CHF 562.7 ± 93.34 ng/ml vs. controls 245.3 ± 58.19 ng/ml; p = 0.02) as well as renal and heart tissue NGAL levels [CHF 70,680 ± 4,337 arbitrary units (AU) vs. controls 32,120 ± 4,961 AU; p = 0.001] rose significantly, and they were found to be complexed with MMP9 in CHF rats. A higher number of kidney TUNEL-positive tubular cells was also detected (CHF 114.01 ± 45.93 vs. controls 16.36 ± 11.60 cells/mm²; p = 0.0004). Conclusion: In this model of CHF with prevalent congestion, kidney injury is characterized by tubular damage and systemic inflammation. The upregulated NGAL complexed with MMP9 perpetuates the vicious circle of kidney/heart damage by enhancing the enzymatic activity of MMP9 with extracellular matrix degradation, worsening heart remodeling.

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“…Analytical SDS page was performed on 7% polyacrylamide slabs with 37.5% vol/vol glycerol to separate MHCs. The percent distribution of the MHCs was determined by a densitometric scan (Sigma Gel, SPSS, Chicago, IL, USA) after image acquisition of the stained gels [19,20].…”

Section: Myosin Heavy Chains (Mhcs) Determinationmentioning

confidence: 99%