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High blood pressure, cardiac hypertrophy, heart failure and dystrophin-glycoprotein complex


Cardiac hypertrophy is an adaptive morphological response of the heart to work overload and is an important risk factor for myocardial infarction, congestive heart failure and sudden death. Cardiac hypertrophy in response to pressure overload is initially a beneficial response and the mechanisms responsible for transition from physiological cardiac hypertrophy or compensated hypertrophy to pathological or decompensated hypertrophy are still partially defined. Although fibrosis and hypertrophy of cardiomyocytes are considered the main markers of abnormal heart failure, one intriguing possibility is that the mechanical properties of cardiomyocytes themselves are changed. The obvious candidates for this possible remodeling are the intracellular cytoskeletal proteins. Recently, attention has been given to the cytoskeletal proteins that are involved in anchoring the myofibrils to the extracellular matrix via transmembrane proteins: the dystrophin- glycoproteins complex (dystroglycan, sarcoglycan, sarcospan, dystrobrevin and sintrofinas); connection talina-integrin-and vinculin spectrin-binding inner surface of the cell membrane. The organization and interaction among these structural proteins are important for understanding the cellular mechanisms involved in the mechanical dysfunction observed in cardiomyopathies. Thus, the different compartments of the cytoskeleton might be directly involved in the development of cardiac hypertrophy and in the progression from compensated hypertrophy to failure. Because of this, the importance of molecular changes related to cardiac hypertrophy lies in the fact that the main changes, which determine the transition of compensated cardiac hypertrophy to failure, can be present even during the hypertrophic stage. Thus, it is essential to define the mechanistic aspects of pathophysiological processes involved in the deterioration of cardiac function and development of strategies to inhibit or reverse the progression of the disease. It is necessary to test the hypothesis that this system of anchoring could change in these situations. Because these changes due to loss of internal organization of the contractile system would represent a gradual collapse due to the presence of hypertension, we have to test antihypertensive drugs in an attempt to reverse these changes. (AU)

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Scientific publications (8)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
CELES, MARA R. N.; MALVESTIO, LYGIA M.; SUADICANI, SYLVIA O.; PRADO, CIBELE M.; FIGUEIREDO, MARIA J.; CAMPOS, ERICA C.; FREITAS, ANA C. S.; SPRAY, DAVID C.; TANOWITZ, HERBERT B.; DA SILVA, JOAO S.; et al. Disruption of Calcium Homeostasis in Cardiomyocytes Underlies Cardiac Structural and Functional Changes in Severe Sepsis. PLoS One, v. 8, n. 7, . (10/13199-1, 09/17787-8, 10/19216-5, 10/18629-4, 09/54010-1, 09/02942-8)
DOS SANTOS, DANIELE O.; BLEFARI, VALDECIR; PRADO, FERNANDA P.; SILVA, CARLOS A.; FAZAN, JR., RUBENS; SALGADO, HELIO C.; RAMOS, SIMONE G.; PRADO, CIBELE M.. Reduced expression of adherens and gap junction proteins can have a fundamental role in the development of heart failure following cardiac hypertrophy in rats. Experimental and Molecular Pathology, v. 100, n. 1, p. 167-176, . (09/17787-8, 10/19216-5, 12/09665-2, 09/54010-1, 14/07527-7)
MALVESTIO, LYGIA M.; CELES, MARA RUBIA N.; JELICKS, LINDA A.; TANOWITZ, HERBERT B.; PRADO, CIBELE M.. Dantrolene improves in vitro structural changes induced by serum from Trypanosoma cruzi-infected mice. Parasitology Research, v. 116, n. 1, p. 429-433, . (10/18629-4, 10/19216-5, 09/17787-8)
PRADO, CIBELE M.; CELES, MARA R. N.; MALVESTIO, LYGIA M.; CAMPOS, ERICA C.; SILVA, JOAO S.; JELICKS, LINDA A.; TANOWITZ, HERBERT B.; ROSSI, MARCOS A.. Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy. Microbes and Infection, v. 14, n. 1, p. 59-68, . (10/13199-1, 09/17787-8, 10/19216-5, 10/18629-4, 09/54010-1)
CAMPOS, ERICA C.; O'CONNELL, JOAO L.; MALVESTIO, LYGIA M.; DIAS ROMANO, MINNA M.; RAMOS, SIMONE G.; CELES, MARA RUBIA N.; PRADO, CIBELE M.; SIMOES, MARCUS V.; ROSSI, MARCOS A.. Calpain-mediated dystrophin disruption may be a potential structural culprit behind chronic doxorubicin-induced cardiomyopathy. European Journal of Pharmacology, v. 670, n. 2-3, p. 541-553, . (10/13199-1, 09/17787-8, 10/19216-5, 09/54010-1, 09/02942-8)
CELES, MARA R. N.; PRADO, CIBELE M.; ROSSI, MARCOS A.. Sepsis: Going to the Heart of the Matter. PATHOBIOLOGY, v. 80, n. 2, p. 70-86, . (10/19216-5, 09/54010-1, 09/17787-8)
MALVESTIO, LYGIA M.; CELES, MARA R. N.; MILANEZI, CRISTIANE; SILVA, JOAO S.; JELICKS, LINDA A.; TANOWITZ, HERBERT B.; ROSSI, MARCOS A.; PRADO, CIBELE M.. Role of dystrophin in acute Trypanosoma cruzi infection. Microbes and Infection, v. 16, n. 9, p. 768-777, . (09/17787-8, 10/19216-5, 10/18629-4)
PRADO, FERNANDA P.; DOS SANTOS, DANIELE O.; BLEFARI, VALDECIR; SILVA, CARLOS A.; MACHADO, JULIANO; KETTELHUT, ISIS DO CARMO; RAMOS, SIMONE G.; BARUFFI, MARCELO DIAS; SALGADO, HELIO C.; PRADO, CIBELE M.. Early dystrophin loss is coincident with the transition of compensated cardiac hypertrophy to heart failure. PLoS One, v. 12, n. 12, . (12/23649-0, 16/21710-4, 09/17787-8, 13/20549-7, 10/19216-5, 09/54010-1)

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