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1.
Clin Cosmet Investig Dermatol ; 16: 1095-1105, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37123622

RESUMEN

Background: Biorevitalization solutions contain numerous nutritive compounds to improve skin quality. Dermal fillers like HA (hyaluronic acid), depending on rheological characteristics, are used to fill large static defaults with a sustained long-term efficacy. Treatments with either dermal filler or biorevitalization solutions alone are not enough to bring a global facial aging approach. Objective: To demonstrate the anti-aging performance and safety of a new protocol, BIONUTRILIFT, which combined an HA-based filler with Tri-Hyal technology and a skin biorevitalizer, to target the skin quality and wrinkles correction at the same time. Materials and Methods: Eligible subjects were enrolled based on a score of 2, 3, 4, or 5 on Bazin cheek folds wrinkle scale. Safety outcomes measured were immediate and local tolerability. Performance outcomes measured included: proportion of subjects in whom the severity of cheeks folds, nasolabial folds, marionette lines, upper lip wrinkles and skin radiance remained at least one point below the baseline measurement (Bazin scale) Global Aesthetic Improvement Scale scores by subjects and investigators. Results: In performance analyses with the combined protocol, skin radiance and cheek folds wrinkle correction sustained during the four-month study and decrease by 61% and 55%, respectively. 96% and 77% of subjects respectively showed at least a one-point decrease in the mean skin radiance score and Bazin score compared with baseline. Interestingly, the BIONUTRILIFT protocol showed the distance effect of vector A (cheek injection) and vector B (mandibular injection) on perioral zone and remained significant even 120 days after injections. Adverse events (AEs) were consistent with the expected AEsthat occurred after dermal injections. No serious AEswere recorded. Conclusion: BIONUTRILIFT may satisfy the subjects' demand by obtaining in the same session a simple, personalized, noninvasive, atraumatic, and reproductible technique.

2.
Front Immunol ; 9: 1243, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29971063

RESUMEN

Optineurin (Optn) is a 577 aa protein encoded by the Optn gene. Mutations of Optn are associated with normal tension glaucoma and amyotrophic lateral sclerosis, and its gene has also been linked to the development of Paget's disease of bone and Crohn's disease. Optn is involved in diverse cellular functions, including NF-κB regulation, membrane trafficking, exocytosis, vesicle transport, reorganization of actin and microtubules, cell cycle control, and autophagy. Besides its role in xenophagy and autophagy of aggregates, Optn has been identified as a primary autophagy receptor, among the five adaptors that translocate to mitochondria during mitophagy. Mitophagy is a selective macroautophagy process during which irreparable mitochondria are degraded, preventing accumulation of defective mitochondria and limiting the release of reactive oxygen species and proapoptotic factors. Mitochondrial quality control via mitophagy is central to the health of cells. One of the important surveillance pathways of mitochondrial health is the recently defined signal transduction pathway involving the mitochondrial PTEN-induced putative kinase 1 (PINK1) protein and the cytosolic RING-between-RING ubiquitin ligase Parkin. Both of these proteins, when mutated, have been identified in certain forms of Parkinson's disease. By targeting ubiquitinated mitochondria to autophagosomes through its association with autophagy related proteins, Optn is responsible for a critical step in mitophagy. This review reports recent discoveries on the role of Optn in mitophagy and provides insight into its link with neurodegenerative diseases. We will also discuss the involvement of Optn in other pathologies in which mitophagy dysfunctions are involved including cancer.


Asunto(s)
Mitocondrias/genética , Mitocondrias/metabolismo , Neoplasias/etiología , Neoplasias/metabolismo , Enfermedades Neurodegenerativas/etiología , Enfermedades Neurodegenerativas/metabolismo , Factor de Transcripción TFIIIA/genética , Factor de Transcripción TFIIIA/metabolismo , Animales , Biomarcadores , Proteínas de Ciclo Celular , Susceptibilidad a Enfermedades , Regulación de la Expresión Génica , Humanos , Proteínas de Transporte de Membrana , Mitofagia/genética , Neoplasias/patología , Enfermedades Neurodegenerativas/patología , Transducción de Señal
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