CV Lattes
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Universidade Estadual Paulista (UNESP). Campus de Botucatu. Instituto de Biociências (IBB) (Institutional affiliation from the last research proposal) Birthplace: Brazil
Renato Ferretti is an Assistant Professor in the Department of Structural and Functional Biology, Anatomy section, at the Institute of Biosciences at UNESP. He holds a degree in Physical Therapy from UNIMEP (2004) and a Master's and PhD in Cellular and Structural Biology from UNICAMP (2012). During his PhD, he was a fellow of the Doctorate Program with an Internship Abroad (PDEE), completing complementary training at the Muscle Institute at the University of Pennsylvania (UPenn) (2010-2011). In teaching, he has experience in Morphology with an emphasis on Human Anatomy. In research, his main research lines include the Structural and Functional Biology of Muscle Tissue and the Mechanisms of Protection against Myonecrosis in Experimental Models of Duchenne Muscular Dystrophy. Research on muscle tissue has a direct impact on public health, both for the general population and for patients with muscular diseases. (Source: Lattes Curriculum)
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In Duchenne muscular dystrophy (DMD) and in the mdx mice, the experimental model of DMD, the lack of dystrophin leads to muscle necrosis and progressive cardiorespiratory failure. The absence of dystrophin leads to a decrease in expression of dystrophin-glycoprotein complex (DGC) and loss of homeostasis of calcium (Ca2+), resulting in myonecrosis. MicroRNAs (miRs), non-coding RNAs, appear…
Despite the absence of the dystrophin protein causing Duchenne muscular dystrophy (DMD), secondary events such as increased calcium (Ca2+) levels, inflammation, and reactive oxygen and nitrogen species (RONS) are correlated with the worsening of the Duchenne muscular dystrophy (DMD) phenotype. These events trigger the reduction and/or functional loss of ventilation. Increased intracellula…
In the absence of dystrophin, muscle fibers undergo membrane rupture, releasing damage-associated molecular patterns (DAMPs), which leads to elevated serum creatine kinase (CK) levels, inflammation (characterized by increased TNF-¿ levels), and ultimately functional loss. The mdx mouse model, which mimics Duchenne muscular dystrophy (DMD), presents muscle fibers lacking dystrophin, result…
There is no curative treatment for Duchenne muscular dystrophy (DMD) which is a severe and progressive X-linked muscle disease caused by loss of dystrophin. DMD is associated with muscle degeneration, necrosis, inflammation, fat replacement and fibrosis, which results in muscle weakness, cardiorespiratory failure and premature death. The most important secondary event is the abnormal elev…
Duchenne muscular dystrophy (DMD) is a severe, progressive, X-linked muscle disease caused by the loss of dystrophin. DMD is associated with muscle necrosis, degeneration, inflammation, fat replacement, and fibrosis, resulting in muscle weakness, cardiorespiratory failure, and premature death. There is no curative therapy. Investigations into disease mechanisms offer an opportunity to ide…
Duchenne muscular dystrophy (DMD) is characterized by a progressive muscle disorder related to lack of dystrophin protein with increased Ca2+ uptake in the muscle fibers leading to muscle fiber necrosis, myonecrosis. Ca2+-operated channel entry (SOCE) belong to a complex of selective Ca2+ channels in the sarcolemma, including Orai1 and STIM1, which are present in the sarcoplasmic reticulu…
| 1 / 1 | Completed research grants |
| 2 / 2 | Ongoing scholarships in Brazil |
| 3 / 3 | Completed scholarships in Brazil |
| 6 / 6 | All research grants and scholarships |
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