Estrada Mena, Francisco Javier
Main Affiliation
Preferred name
Estrada Mena, Francisco Javier
Official Name
Estrada Mena, Francisco Javier
ORCID
0000-0002-0833-3630
Researcher ID
AAI-2437-2020
Scopus Author ID
57192982524
32 results
Now showing 1 - 10 of 32
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Item type:Publication, Preparation of Mouse Embryonic Eye Sections for Routine Histology(Springer US, 2026); ; Ramírez-Sánchez, Israel - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Novel genome-wide associations for age-related macular degeneration in the sarcoglycan-sarcospan protein complex(2020)19 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Altered calcium pump and secondary deficiency of γ-sarcoglycan and microspan in sarcoplasmic reticulum membranes isolated from δ-sarcoglycan knockout mice(2010)Scopus© Citations 11 11 1 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, A new de novo mutation in a non-hot spot region at the DMD gene in a Mexican family(2015)6 1 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Brief inflammatory profile after femtosecond laser-assisted pretreatment in nuclear cataract surgery(2020)33 1 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Lack of Delta-Sarcoglycan (Sgcd) Results in Retinal Degeneration(2019); ; Age-related macular degeneration (AMD) is the leading cause of central vision loss and severe blindness among the elderly population. Recently, we reported on the association of the SGCD gene (encoding for δ-sarcoglycan) polymorphisms with AMD. However, the functional consequence of Sgcd alterations in retinal degeneration is not known. Herein, we characterized changes in the retina of the Sgcd knocked-out mouse (KO, Sgcd−/−). At baseline, we analyzed the retina structure of three-month-old wild-type (WT, Sgcd+/+) and Sgcd−/− mice by hematoxylin and eosin (H&E) staining, assessed the Sgcd-protein complex (α-, β-, γ-, and ε-sarcoglycan, and sarcospan) by immunofluorescence (IF) and Western blot (WB), and performed electroretinography. Compared to the WT, Sgcd−/− mice are five times more likely to have retinal ruptures. Additionally, all the retinal layers are significantly thinner, more so in the inner plexiform layer (IPL). In addition, the number of nuclei in the KO versus the WT is ever so slightly increased. WT mice express Sgcd-protein partners in specific retinal layers, and as expected, KO mice have decreased or no protein expression, with a significant increase in the α subunit. At three months of age, there were no significant differences in the scotopic electroretinographic responses, regarding both a- and b-waves. According to our data, Sgcd−/− has a phenotype that is compatible with retinal degeneration. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.Scopus© Citations 5 30 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins(2024); Laura Sánchez-Chapul<jats:p>Muscular dystrophies (MDs) are a heterogeneous group of diseases of genetic origin characterized by progressive skeletal muscle degeneration and weakness. There are several types of MDs, varying in terms of age of onset, severity, and pattern of the affected muscles. However, all of them worsen over time, and many patients will eventually lose their ability to walk. In addition to skeletal muscle effects, patients with MDs may present cardiac and respiratory disorders, generating complications that could lead to death. Interdisciplinary management is required to improve the surveillance and quality of life of patients with an MD. At present, pharmacological therapy is only available for Duchene muscular dystrophy (DMD)—the most common type of MD—and is mainly based on the use of corticosteroids. Other MDs caused by alterations in dystrophin-associated proteins (DAPs) are less frequent but represent an important group within these diseases. Pharmacological alternatives with clinical potential in patients with MDs and other proteins associated with dystrophin have been scarcely explored. This review focuses on drugs and molecules that have shown beneficial effects, mainly in experimental models involving alterations in DAPs. The mechanisms associated with the effects leading to promising results regarding the recovery or maintenance of muscle strength and reduction in fibrosis in the less-common MDs (i.e., with respect to DMD) are explored, and other therapeutic targets that could contribute to maintaining the homeostasis of muscle fibers, involving different pathways, such as calcium regulation, hypertrophy, and maintenance of satellite cell function, are also examined. It is possible that some of the drugs explored here could be used to affordably improve the muscular function of patients until a definitive treatment for MDs is developed.</jats:p>4 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Detección de una mutación en el gen KCNQ1 (KvLQT1) causante de síndrome de Jervell, Lange-Nielsen en una familia mexicana(2006-07); Scopus© Citations 7 13 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Machine learning method to establish the connection between age related macular degeneration and some genetic variations(2016); ; Scopus© Citations 1 56 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, FMR1 CGG repeat distribution and linked microsatellite-SNP haplotypes in normal Mexican Mestizo and indigenous populations(2006)13 2