Cibele Maria Prado Zinni
CV Lattes
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Universidade de São Paulo (USP). Faculdade de Zootecnia e Engenharia de Alimentos (FZEA) (Institutional affiliation for the last research proposal) Birthplace: Brazil
graduation at Ciências Biológicas Modalidade Médica from Centro Universitário Herminio Ometto de Araras (2000) and doctorate at Patologia Experimental e Comparada from Universidade de São Paulo, Campus Ribeirão Preto (2006). Has experience in Medicine, focusing on Pathological Anatomy and Clinical Pathology, acting on the following subjects: atherosclerosis, hypertension, cardiac remodeling, heart failure, cardiac hypertrophy, Chagas disease, sepsis. (Source: Lattes Curriculum)
- Analysis of circulating miRNA levels at the transition from compensated cardiac hypertrophy to heart failure: identification of possible biomarkers of heart failure, AP.R
Abstract
Heart failure (HF) is a complex clinical syndrome that can arise as a consequence of a broad spectrum of structural and functional cardiac abnormalities. Cardiac hypertrophy as a consequence of hypertension is a compensatory mechanism that initially protects the heart, but excessive work overload is an important predictor of HF. Despite the importance of hypertrophy as a risk factor for...
- High blood pressure, cardiac hypertrophy, heart failure and dystrophin-glycoprotein complex, AP.JP
Abstract
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...
- 15th Annual Meeting of the European Council for Cardiovascular Research, AR.EXT
- Turbulent blood flow plays an essential localizing role in the development of atherosclerotic lesions in experimentally induced., PUB.ART
Abstract
Taking into account that atherosclerosis is a focal disease and high levels of plasma cholesterol are closely correlated with its pathogenesis, it is a challenge to explain how equal concentrations of cholesterol bathing the endothelium can produce local rather than global effects on arteries. The focal distribution of atherosclerotic lesions has been considered to be dependent, at leas...
- The role of TGF-b in the transition of compensated to decompensated heart hypertrophy in rats submitted to abdominal aorta constriction, BP.IC
Abstract
Cardiac hypertrophy is an adaptive morphological response of the heart to work overload and is an important risk factor for myocardial infarction, heart failure and sudden death. Cardiac hypertrophy in response to pressure overload is initially a beneficial response and the mechanisms responsible for the transition of compensated cardiac hypertrophy or physiological to decompensated hyp...
- High blood pressure, cardiac hypertrophy, heart failure and dystrophin glycoprotein complex, BP.IC
Abstract
The aim of this work is the study of hypertensive heart disease, heart failure and cardiac hypertrophy, and cytoskeletal proteins. Specifically, we will evaluate a group of structural proteins responsible for the connection between the intracellular and extracellular environment and provide structural stability to the cell membrane of the cardiomyocytes. The absence of one or more compo...
- Hypertension, cardiac hypertrophy and cardiac failure and dystrophin glycoproteins, BP.JP
- Possible role of dystrophin and integrin-associated glycoprotein complex in sudden death in experimental Chagas disease, BE.PQ
Abstract
Chagas' disease, caused by the protozoan flagellate Trypanosoma cruzi infection, is endemic in 21 countries of South and Central Americas. The transmission via insects has been efficiently controlled in affected areas and blood transfusion and congenital infection are the most important sources of the disease in humans. Experimental production of Chagas' disease through infection of mic...
| 1 / 1 | Ongoing research grants |
| 4 / 3 | Completed research grants |
| 5 / 3 | Completed scholarships in Brazil |
| 1 / 1 | Completed scholarships abroad |
| 11 / 8 | All research grants and scholarships |
| Associated processes | |
(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)
| Publications | 12 |
| Citations | 195 |
| Cit./Article | 16.3 |
| Data from Web of Science | |
CELES, MARA RUBIA N.; TORRES-DUENAS, DIEGO; MALVESTIO, LYGIA M.; BLEFARI, VALDECIR; CAMPOS, ERICA C.; RAMOS, SIMONE G.; PRADO, CIBELE M.; CUNHA, FERNANDO Q.; ROSSI, MARCOS A.. Disruption of sarcolemmal dystrophin and beta-dystroglycan may be a potential mechanism for myocardial dysfunction in severe sepsis. LABORATORY INVESTIGATION, v. 90, n. 4, p. 531-542, APR 2010. Web of Science Citations: 14.
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, JAN 2012. Web of Science Citations: 7. (10/19216-5, 10/18629-4, 10/13199-1, 09/54010-1, 09/17787-8)
ROSSI‚ M.A.; TANOWITZ‚ H.B.; MALVESTIO‚ L.M.; CELES‚ M.R.; CAMPOS‚ E.C.; BLEFARI‚ V.; PRADO‚ C.M.. Coronary microvascular disease in chronic Chagas cardiomyopathy including an overview on history‚ pathology‚ and other proposed pathogenic mechanisms. PLoS Neglected Tropical Diseases, v. 4, n. 8, p. e674, 2010. (08/00954-6)
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, 2013. Web of Science Citations: 46. (09/54010-1, 09/17787-8, 10/19216-5)
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, NOV 30 2011. Web of Science Citations: 20. (10/19216-5, 10/13199-1, 09/54010-1, 09/02942-8, 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, SEP 2014. Web of Science Citations: 3. (10/18629-4, 10/19216-5, 09/17787-8)
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, FEB 2016. Web of Science Citations: 6. (10/19216-5, 09/17787-8, 14/07527-7, 12/09665-2, 09/54010-1)
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, JUL 23 2013. Web of Science Citations: 18. (10/19216-5, 09/17787-8, 10/18629-4, 10/13199-1, 09/54010-1, 09/02942-8)
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, JAN 2017. Web of Science Citations: 2. (10/19216-5, 09/17787-8, 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, DEC 21 2017. Web of Science Citations: 2. (10/19216-5, 09/17787-8, 16/21710-4, 13/20549-7, 09/54010-1, 12/23649-0)
ROSSI, MARCOS A.; TANOWITZ, HERBERT B.; MALVESTIO, LYGIA M.; CELES, MARA R.; CAMPOS, ERICA C.; BLEFARI, VALDECIR; PRADO, CIBELE M.. Coronary Microvascular Disease in Chronic Chagas Cardiomyopathy Including an Overview on History, Pathology, and Other Proposed Pathogenic Mechanisms. PLoS Neglected Tropical Diseases, v. 4, n. 8, AUG 2010. Web of Science Citations: 40. (08/00954-6)
CELES, MARA R. N.; TORRES-DUENAS, DIEGO; PRADO, CIBELE M.; CAMPOS, ERICA C.; MOREIRA, JORGE E.; CUNHA, FERNANDO Q.; ROSSI, MARCOS A.. INCREASED SARCOLEMMAL PERMEABILITY AS AN EARLY EVENT IN EXPERIMENTAL SEPTIC CARDIOMYOPATHY: A POTENTIAL ROLE FOR OXIDATIVE DAMAGE TO LIPIDS AND PROTEINS. Shock, v. 33, n. 3, p. 322-331, MAR 2010. Web of Science Citations: 20.
PRADO, CIBELE M.; FINE, EUGENE J.; KOBA, WADE; ZHAO, DAZHI; ROSSI, MARCOS A.; TANOWITZ, HERBERT B.; JELICKS, LINDA A.. Micro-Positron Emission Tomography in the Evaluation of Trypanosoma cruzi-Induced Heart Disease: Comparison with Other Modalities. American Journal of Tropical Medicine and Hygiene, v. 81, n. 5, p. 900-905, NOV 2009. Web of Science Citations: 17. (08/00954-6)