Armando Martinez Salazar
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Armando Martinez Salazar has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Edwin Peguero
Department of Neurology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
1 shared publication - Muhammad Jaffer
Department of Neurology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
1 shared publication - Sepideh Mokhtari
Department of Neuro-oncology, The H. Lee Moffitt Cancer Center, Tampa, FL, USA
1 shared publication
Latest Publications
- Open Access
The Role of Complement in the Pathogenesis and Treatment of Myasthenia Gravis
Myasthenia gravis is an antibody-mediated autoimmune condition characterized by defects in cholinergic transmission at the neuromuscular junction. In AchR antibody-positive patients, complement activation plays a prominent role in the disease process, which appears to be mediated by the activation of the membrane attack complex. Since IgG4 is not a good complement activator, the role of complement in MuSK antibody-positive myasthenia gravis patients is negligible. Experimental animal models of myasthenia gravis have shown promise with the antagonism of different elements of the complement cascade, with positive clinical outcomes. This has led to the development of the first C5 inhibitors approved for myasthenia gravis with AchR antibodies: eculizumab, ravulizumab, and zilucoplan. Other clinical trials are currently in progress, investigating the potential therapeutic role of other targets, including the Factor B inhibition or hepatic synthesis of the C5 protein. Other proposed potential targets that have not yet been clinically tested are also discussed in this review article.
Open AccessThe Role of Complement in the Pathogenesis and Treatment of Myasthenia Gravis
Myasthenia gravis is an antibody-mediated autoimmune condition characterized by defects in cholinergic transmission at the neuromuscular junction. In AchR antibody-positive patients, complement activation plays a prominent role in the disease process, which appears to be mediated by the activation of the membrane attack complex. Since IgG4 is not a good complement activator, the role of complement in MuSK antibody-positive myasthenia gravis patients is negligible. Experimental animal models of myasthenia gravis have shown promise with the antagonism of different elements of the complement cascade, with positive clinical outcomes. This has led to the development of the first C5 inhibitors approved for myasthenia gravis with AchR antibodies: eculizumab, ravulizumab, and zilucoplan. Other clinical trials are currently in progress, investigating the potential therapeutic role of other targets, including the Factor B inhibition or hepatic synthesis of the C5 protein. Other proposed potential targets that have not yet been clinically tested are also discussed in this review article.