ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
A Novel Reactive Oxygen Species-Responsive Bone-Targeted Nanoplatform Based on Cloperastine Attenuates Ovariectomy-Induced Bone Loss by Inhibiting Osteoclast Oxidative Phosphorylation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Postmenopausal osteoporosis is caused by excessive osteoclast-mediated bone resorption. This study identifies mitochondrial oxidative phosphorylation (OXPHOS) as a tractable metabolic target for antiresorptive therapy. A literature-guided drug repurposing screen focused on compounds reported to affect OXPHOS or related energy metabolism identified cloperastine (Clo) as a potent suppressor of receptor activator of nuclear factor κB ligand-induced osteoclastogenesis. Clo reduces mitochondrial respiration, downregulates OXPHOS complex proteins, decreases mitochondrial reactive oxygen species (ROS), dissipates the mitochondrial membrane potential, disrupts mitochondrial dynamics, and collectively impairs osteoclast differentiation and bone resorption in vitro. Asp8-modified methionine/lysine-based ROS-responsive polyethylene glycol micelles encapsulating Clo (Clo/Asp8-PMK-MCs) were developed for potential bone-directed delivery. These micelles (∼220 nm; -3.60 ± 0.09 mV) exhibit ROS-triggered disassembly and accelerated Clo release under oxidative conditions. Fluorescence tracking of DID-labeled micelles shows stronger skeletal signals with Asp8 modification than without it. Clo/Asp8-PMK-MCs inhibit osteoclast differentiation and bone resorption, whereas bioactive Asp8-PMK-MCs simultaneously promote osteoblast differentiation and matrix mineralization. In ovariectomized mice, Clo/Asp8-PMK-MCs attenuate ovariectomy-induced bone loss, preserve trabecular bone microarchitecture, reduce osteoclast-related parameters and serum bone resorption markers, and enhance bone formation. These findings support Clo/Asp8-PMK-MCs as a potential OXPHOS-targeted nanomedicine integrating Clo-mediated antiresorptive activity with carrier-mediated osteogenic activity to attenuate estrogen deficiency-induced bone loss.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.