Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors.
Sandra Freitas-RodríguezDepartamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain.ORCID https://orcid.org/0000-0001-5733-9839
Alejandra Valle-CaoDepartamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain.ORCID https://orcid.org/0000-0002-1962-9728
Manuel Fernández-SanjurjoDepartamento de Biología Funcional, Área de Fisiología, Facultad de Medicina, Universidad de Oviedo, Oviedo, Spain.
Benjamín Fernández-GarcíaDepartamento de Morfología y Biología Celular, Facultad de Medicina, Universidad de Oviedo, Oviedo, Spain.ORCID https://orcid.org/0000-0002-2391-680X
Vanessa LoredoDepartamento de Medicina, Área de Pediatría, Facultad de Medicina, Universidad de Oviedo, Oviedo, Spain.
María Teresa Fernández-GarcíaUnidad de Histopatología Molecular, IUOPA, Universidad de Oviedo, Oviedo, Spain.
Alejandro LuciaDepartment of Sport Sciences, Faculty of Medicine, Health and Sports, Universidad Europea de Madrid, Madrid, Spain.
Carlos López-OtínDepartamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain.
Alejandro López-SotoDepartamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain.ORCID https://orcid.org/0000-0002-6360-5205
Alicia R FolguerasDepartamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, Oviedo, Spain.ORCID https://orcid.org/0000-0003-3426-9502
Funding
Agencia de Ciencia, Competitividad Empresarial e Innovación Asturiana-SEKUENS GRU-GIC-24-103Consejería de Ciencia, Innovación y Universidad del Gobierno del Principado de Asturias AYUD/2021/51062European Research Council 742067, DeAge, ERC-2016-ADGMinisterio de Ciencia e Innovación PID2021-126372OB-I00Ministerio de Ciencia e Innovación RTI2018-096479-A-I00
6 · The paper itself
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by the early development of pathological features associated with aging, ultimately leading to premature death. HGPS primarily affects tissues of mesenchymal origin, as evidenced by the clinical manifestations characteristic of this premature aging disorder, including, but not limited to, osteoporosis, muscle wasting, lipodystrophy, and cardiovascular disease. In this study, we used preclinical mouse models and both genetic and translational approaches to investigate whether an antiresorptive strategy, based on RANKL targeting, ameliorated the bone loss phenotype of progeroid mice. Here we show that osteocyte-derived RANKL deletion in the Zmpste24
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Targeting RANKL Prevents Bone Loss, Improves Muscle Function and Extends Lifespan in Progeroid Mice. · full record | OpenQuestion