Jorge Esteve-Girbés
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jorge Esteve-Girbés has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Alicia Navarro-Sempere
Immunology, Cellular and Developmental Biology Group, Department of Biotechnology, University of Alicante, Ap. 99, E-03080 Alicante, Spain
1 shared publication - Ana Belen Lopez Jaen
Department of Biotechnology, University of Alicante, 03690 San Vicente del Raspeig, Spain
1 shared publication - Carolina Pujalte-Satorre
Immunology, Cellular and Developmental Biology Group, Department of Biotechnology, University of Alicante, Ap. 99, E-03080 Alicante, Spain
1 shared publication - Francisco J. Navarro-Blasco
Department of Biotechnology, University of Alicante, 03690 San Vicente del Raspeig, Spain
1 shared publication - José Miguel Sempere-Ortells
Immunology, Cellular and Developmental Biology Group, Department of Biotechnology, University of Alicante, Ap. 99, E-03080 Alicante, Spain
1 shared publication - Juan Javaloyes-Antón
Department of Physics, Systems Engineering and Signal Theory, University of Alicante, 03690 San Vicente del Raspeig, Spain
1 shared publication
Latest Publications
- Open Access
- 25 January 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (3) , 1506
Exosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches
Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine.
- 25 January 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (3) , 1506
Open AccessExosomal Osteoclast-Derived miRNA in Rheumatoid Arthritis: From Their Pathogenesis in Bone Erosion to New Therapeutic Approaches
Rheumatoid arthritis (RA) is an autoimmune disease that causes inflammation, pain, and ultimately, bone erosion of the joints. The causes of this disease are multifactorial, including genetic factors, such as the presence of the human leukocyte antigen (HLA)-DRB1*04 variant, alterations in the microbiota, or immune factors including increased cytotoxic T lymphocytes (CTLs), neutrophils, or elevated M1 macrophages which, taken together, produce high levels of pro-inflammatory cytokines. In this review, we focused on the function exerted by osteoclasts on osteoblasts and other osteoclasts by means of the release of exosomal microRNAs (miRNAs). Based on a thorough revision, we classified these molecules into three categories according to their function: osteoclast inhibitors (miR-23a, miR-29b, and miR-214), osteoblast inhibitors (miR-22-3p, miR-26a, miR-27a, miR-29a, miR-125b, and miR-146a), and osteoblast enhancers (miR-20a, miR-34a, miR-96, miR-106a, miR-142, miR-199a, miR-324, and miR-486b). Finally, we analyzed potential therapeutic targets of these exosomal miRNAs, such as the use of antagomiRs, blockmiRs, agomiRs and competitive endogenous RNAs (ceRNAs), which are already being tested in murine and ex vivo models of RA. These strategies might have an important role in reestablishing the regulation of osteoclast and osteoblast differentiation making progress in the development of personalized medicine.