ArticleCalcified tissue international2026
The Alamandine/MrgprD as a Key Player in Antiresorptive Effects in an Osteoporosis Experimental Model.
Article in Calcified tissue international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The renin-angiotensin system plays a key role in bone metabolism. While the classical renin-angiotensin system axis promotes bone resorption, the counter-regulatory axis, including alamandine via MrgprD receptor, favors bone formation. This study evaluated the therapeutic effects of alamandine in a model of osteoporosis. In vitro, alamandine reduced osteoclast activation and size in a MrgprD receptor-dependent manner. In vivo, ovariectomy-induced osteoporosis reduced bone parameters, and alamandine reversed trabecular bone loss in wild-type mice but not in MrgprD knockout mice, demonstrating the essential role of the receptor. Alamandine also reduced serum calcium and phosphorus levels in ovariectomized wild-type mice, with no effect on ovariectomized knockout animals. Furthermore, modulation of iron levels differed between genotypes, suggesting the involvement of ferroptosis-related pathways. Histological analysis revealed an increase in the number of osteoblasts and osteocytes in wild-type mice treated with alamandine, corroborating its role in osteogenic differentiation, possibly via the AMPK/eNOS pathway. In contrast, alamandine exacerbated bone resorption in ovariectomized MrgprD knockout mice, potentially through alternative renin-angiotensin system receptors. In conclusion, alamandine increases bone formation and reduces resorption through MrgprD receptor signaling, highlighting its potential as a therapeutic agent in osteoporosis.
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