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The Receptor for Advanced Glycation End-products (RAGE) is a pattern recognition receptor (PRR) present at very low levels in most tissues in homeostasis, with the exception of the lung, which exhibits high basal expression of RAGE. The identification of protective molecules that allow the heart to “age slowly” could lead to new therapeutic approaches reducing the risk of CVD onset. The activation and proliferation of cardiac fibroblasts (CFs), the main regulators of extracellular matrix (ECM) turnover, are the prominent cause of the progressive myocardial fibrosis occurring during aging. During aging, the heart undergoes anatomical changes characterized by alterations in volume and stiffness, attributable to cardiomyocytes (CM) hypertrophy and interstitial fibrosis, with consequent decline in the diastolic function. However, intrinsic cardiac aging is per se a risk factor and, by making the heart more vulnerable to stress, contributes to increased CV mortality and morbidity. The exponential increase of cardiovascular (CV) diseases (CVD) in the elderly population, including coronary artery disease (CAD), left ventricular hypertrophy and heart failure (HF), is largely ascribable to the long-term exposure to CV risk factors present in later life, like hypertension and diabetes. Keywords: sRAGE, aging, fibrosis, heart failure, cardiac remodeling Introduction Hence, our work shows that RAGE associates with age-dependent myocardial changes and indicates sRAGE as an inhibitor of cardiac fibroblasts differentiation and age-dependent cardiac fibrosis. Finally, sRAGE administration to MA WT animals reduced cardiac fibrosis. Human cardiac fibroblasts stimulated with sRAGE exhibited a reduction in proliferation, pro-fibrotic proteins and TGF-beta Receptor 1 (TGFbR1) expression and Smad2-3 activation. RAGE isoforms were undetectable in LV of WT mice, nevertheless, circulating sRAGE declined with aging and inversely associated with LV diastolic dimensions. Rage-/- mice showed higher fibrosis and a larger number of α-Smooth Muscle Actin (SMA)+ cells with age, along with increased expression of pro-fibrotic Transforming Growth Factor (TGF)-β1 pathway components.
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While aging, Rage-/- mice displayed an increase in left ventricle (LV) dimensions compared to age-matched WT animals, with the main differences observed in the MA groups. We analyzed the cardiac function of three different age groups of female Rage-/- and C57BL/6N (WT) mice: 2.5- (Young), 12- (Middle-age, MA) and 21-months (Old) old. This study aims at investigating RAGE contribution to age-related cardiac remodeling. The soluble isoform (sRAGE) acts as a scavenger blocking the membrane-bound receptor activation. The Receptor for Advanced Glycation End-products (RAGE) is involved in age-related disorders. Myocardial aging increases the cardiovascular risk in the elderly. #Department of Cœur-Vaisseaux, Laboratory of Cardiovascular Research, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. *These authors contributed equally to this work. Chromatin Dynamics Unit, San Raffaele University and IRCCS San Raffaele Hospital, Milan, Italy. Unit of Immunology and Functional Genomics, Centro Cardiologico Monzino-IRCCS, Milan, Italy.Ħ. Department of Biosciences, University of Milan, Milan, Italy.ĥ. Unit of Biostatistics, Centro Cardiologico Monzino-IRCCS, Milan, Italy.Ĥ. Vascular Biology and Regenerative Medicine Unit, Centro Cardiologico Monzino-IRCCS, Milan, Italy.ģ. Unit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino-IRCCS, Milan, Italy.Ģ.
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Tedesco 3, Patrizia Nigro 2, Genny Degani 4, Elisa Gambini 2, Fabrizio Veglia 3, Laura Popolo 4, Giulio Pompilio 2, Gualtiero I. Research Paper Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosisįrancesco Scavello 1*, Filippo Zeni 1*, Giuseppina Milano 2#, Federica Macrì 1, Stefania Castiglione 1, Estella Zuccolo 1, Alessandro Scopece 2, Giovanni Pezone 1, Calogero C.