Growth differentiation factor 15 (GDF-15) in patients admitted for acute heart failure: results from the RELAX-AHF study

2015 ◽  
Vol 17 (11) ◽  
pp. 1133-1143 ◽  
Author(s):  
Gad Cotter ◽  
Adriaan A. Voors ◽  
Margaret F. Prescott ◽  
G. Michael Felker ◽  
Gerasimos Filippatos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor

scholarly journals Dynamics of growth differentiation factor 15 in acute heart failure

2021 ◽  
Author(s):  
Patrícia Lourenço ◽  
Filipe M. Cunha ◽  
João Ferreira‐Coimbra ◽  
Isaac Barroso ◽  
João‐Tiago Guimarães ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor

Growth Differential Factor 15 (GDF%15), Possible Biomarker in Heart Failure

2017 ◽  
Vol 68 (3) ◽  
pp. 631-634
Author(s):  
Valeriu Gabi Dinca ◽  
Gheorghe Manole ◽  
Daniel Cochior ◽  
Alexandra Ligia Dinca
Keyword(s):  
Heart Failure ◽  
Serum Concentration ◽  
The Other ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor ◽  
Other Hand ◽  
The One ◽  
Growth Differential

The present study aims at determining on the one hand the growth differentiation factor 15 significance as possible risk biomarker for this condition and, on the other hand, the degree of correlation between its serum concentration and the class of inotropism deficit.The value of the current research stems from the very selected theme, the activity of GDF-15, member of the superfamily of cytokines TGF-b recognized as having implication in atherosclerosis, but almost unexplored as role in the myocardiumremodeling processes, more precisely in fibrosis.

scholarly journals Growth differentiation factor‐15, treatment with liraglutide, and clinical outcomes among patients with heart failure

2021 ◽  
Author(s):  
Abhinav Sharma ◽  
Stephen Greene ◽  
Muthiah Vaduganathan ◽  
Marat Fudim ◽  
Andrew P. Ambrosy ◽  
...  
Keyword(s):  
Heart Failure ◽  
Clinical Outcomes ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor ◽  
Patients With Heart Failure

Abstract P330: Growth Differentiation Factor 15 Causes Cardiac Cachexia In Heart Failure

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Da Young Lee ◽  
Zhe Jiao ◽  
Andrew Antolic ◽  
Daiana Weiss ◽  
M. Neale Weitzmann ◽  
...  
Keyword(s):  
Heart Failure ◽  
Food Intake ◽  
Cardiac Fibrosis ◽  
Lean Tissue ◽  
Tissue Mass ◽  
Lean Tissue Mass ◽  
Growth Differentiation Factor 15 ◽  
Tissue Weight ◽  
Reduced Fat ◽  
Differentiation Factor

Background: Cachexia is wasting of normal body tissue and occurs in chronic medical diseases. It is a common complication of heart failure (HF) that is associated with very high mortality. Growth differentiation factor 15 (GDF15) regulates food intake and can cause cancer cachexia. GDF15 is a sensitive biomarker in humans, though its biologic function in HF is unknown. This study investigated the role of GDF15 in HF. Methods: We utilized a genetic mouse model of dilated cardiomyopathy (DCM) caused by a mutation in the phospholamban gene (PLN R9C ). PLN R9C mice have dysregulated cardiac calcium handling (a common feature of nearly all forms of HF) and develop progressive DCM that leads to HF and premature death. Q-PCR and ELISA were performed to assess expression, tissue distribution and circulating levels of GDF15 in PLN R9C and age-matched wild type (WT) mice. A double transgenic mouse was created by crossing our DCM model with a constitutive Gdf15 knock-out (KO). Using this novel model, we quantified food intake, and assessed fat and lean tissue mass by tissue weight at necropsy and by dual-energy X-ray absorptiometry (DXA). Cardiac function was assessed using echocardiography, and histochemistry performed to quantify cardiac fibrosis. Survival was assessed by Kaplan-Meier. Results: GDF15 mRNA (43-fold; p<0.01) and protein (54-fold; p<0.01) were increased in LV tissue, and circulating GDF15 was elevated (8.3-fold; p=0.03) in PLN R9C mice. Gdf15 was expressed at low levels and was not increased in other organs in PLN R9C mice. PLN R9C mice developed cachexia (reduced fat and lean mass by tissue weight, reduced fat mass by DXA vs. WT; p<0.01 for all) and consumed less food (p<0.01 vs. WT). Gdf15 KO in PLN R9C preserved fat and lean tissue mass and resulted in higher food intake (p≤0.01 for all). Gdf15 KO had no effect on cardiac structure or function by echocardiography and PLN R9C / Gdf15 KO mice displayed only a small reduction in cardiac fibrosis relative to PLN R9C mice (3%; p<0.01). Despite this, Gdf15 KO prolonged survival in PLN R9C (29±3 vs. 25±3 weeks; p<0.01). Conclusions: GDF15 is a novel cardiac hormone produced in HF that triggers anorexia and cachexia in HF by an extra-cardiac mechanism.

scholarly journals P602Growth differentiation factor-15 predicts mortality in acute heart failure and cardiogenic shock

2017 ◽  
Vol 38 (suppl_1) ◽  
Author(s):  
W.S. Speidl ◽  
S.P. Kastl ◽  
K.A. Krychtiuk ◽  
M. Lenz ◽  
J. Wojta ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiogenic Shock ◽  
Acute Heart Failure ◽  
Differentiation Factor

5949Interleukin-6 and growth differentiation factor-15 in hypertensive heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Fernandez ◽  
J Rysa ◽  
J Nilsson ◽  
G Engstrom ◽  
M Orho-Melander ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transforming Growth Factor ◽  
Mechanical Stretch ◽  
Neonatal Rat ◽  
Chronic Hypertension ◽  
Mrna Levels ◽  
Growth Differentiation Factor 15 ◽  
Hypertrophic Growth ◽  
Differentiation Factor ◽  
Circulating Levels

Abstract Background Hypertension is the leading cause for the development of heart failure (HF). Increased hemodynamic load, including mechanical stretch and neurohumoral factors, is able to trigger hypertrophic growth of cardiac myocytes. Although hypertensive HF is prevalent, there is no useful biomarker to identify HF due to chronic hypertension. Aims To identify plasma markers associated with incidence of hypertensive HF. Methods Circulating levels of 149 proteins were measured by proximity extension assay at baseline examination in 4469 individuals from the Malmö Diet and Cancer study. Protein levels were compared to stretch-activated gene expression changes in cultured neonatal rat ventricular myocytes (NRVM) in response to 1, 4, 12, 24 or 48 hours of cyclic mechanical stretch. Association between plasma proteins level and HF incidence and hypertension was studied using respectively Cox proportional hazards model and binary logistic regressions. Results After Bonferroni correction, 44 circulating proteins were significantly differentially expressed in individuals who developed HF during follow-up versus controls (P<3.4E-4). Out of these, 5 proteins (Interleukin-6 (IL-6), Growth Differentiation Factor-15 (GDF15), Interleukin-1 Receptor-Like-1 (ST2), Plasminogen Activator Urokinase Receptor (U-PAR), Transforming Growth Factor-α (TGF-α)), corresponding mRNA levels were upregulated by mechanical stretch in NRVM at all time points (P<0.05). Similar upregulation for the 5 proteins was shown in hypertensive versus normotensive individuals (P≤8.05E-4). In a model with all 5 proteins entered simultaneously, GDF15 and IL-6 were predictive of incident HF after adjustment for age, sex and NT-BNP levels (205 events; hazard ratio [HR] per SD increment of protein: HR=1.29, CI=1.05–1.58, P=0.013 and HR=1.16, CI=1.02–1.33, P=0.028). Using the same model, IL-6 but not GDF15 associated with hypertension (Odds ratio [OR] per SD increment of IL-6: OR=1.18, CI=1.09–1.27, P=3.3E-5). In hypertensive individuals GDF15 and IL-6 were individually predictive of future HF after adjustment for age, sex, NT-BNP levels, smoking, BMI and diabetes (183 events; HR=1.36, CI=1.16–1.60, P=1.64E-4 and HR=1.21, CI=1.05–1.40, P=0.008). Furthermore, in these hypertensive individuals, GDF15 and IL-6 were predictive of HF in a model with IL-6, GDF15, ST2 and TGF-α entered simultaneously after adjustment for age, sex and NT-BNP levels (176 events; HR=1.36, CI=1.13–1.64, P=0.001 and HR=1.16, CI=1.01–1.34, P=0.041). Conclusions Circulating levels of IL-6 and GDF15 might be used as NT-BNP independent biomarkers for HF development in hypertensive patients. Acknowledgement/Funding Påhlsson, Crafoord, Lundström, Åke Wiberg, Royal Physiographic Society and the Swedish Foundation for Strategic Research for IRC15-0067

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