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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/"><rdf:Description rdf:about="https://dirros.openscience.si/IzpisGradiva.php?id=25209"><dc:title>Potential of synergist ablation to study mechanisms of skeletal muscle hypertrophy in rodent disease models</dc:title><dc:creator>Sarto,	Fabio	(Avtor)
	</dc:creator><dc:creator>Fry,	Christopher S.	(Avtor)
	</dc:creator><dc:creator>Narici,	Marco Vincenzo	(Avtor)
	</dc:creator><dc:creator>Rubin,	Lee L.	(Avtor)
	</dc:creator><dc:creator>Price,	Feodor D.	(Avtor)
	</dc:creator><dc:subject>muscles</dc:subject><dc:subject>cancer cachexia</dc:subject><dc:subject>exercise</dc:subject><dc:subject>metabolic disorders</dc:subject><dc:subject>neuromuscular disorders</dc:subject><dc:subject>resistance training</dc:subject><dc:description>Synergist ablation (SA) is a well-established model of mechanical overload-induced hypertrophy in rodents, commonly used toinfer skeletal muscle adaptation to resistance training in humans. Given the critical role of skeletal muscle atrophy in chronicconditions such as neuromuscular, metabolic, and cardiopulmonary disorders, SA represents a promising preclinical tool tostudy muscle hypertrophy mechanisms in pathological states. However, although extensively characterized in healthy animals,the potential applications of SA in disease models remain largely overlooked. This Mini-Review summarizes existing studiesemploying SA in rodent disease models, highlighting the diverse hypertrophic responses observed across conditions, includ-ing Duchenne muscular dystrophy, obesity, diabetes, cancer cachexia, and chronic kidney disease. Although hypertrophygains are generally attenuated in diseased animals compared to healthy controls, SA-induced overload provides valuableinsights into disease-speciﬁc regulatory mechanisms, including alterations in intracellular signaling, ﬁber type transitions, anddisease phenotype. We also discuss the strengths and limitations of SA as a preclinical model for resistance training in dis-ease contexts and propose its broader adoption for mechanistic investigations into skeletal muscle plasticity under pathologi-cal conditions.</dc:description><dc:date>2025</dc:date><dc:date>2026-01-13 15:45:57</dc:date><dc:type>Neznano</dc:type><dc:identifier>25209</dc:identifier><dc:language>sl</dc:language><dc:rights> Copyright © 2025 The Authors. </dc:rights></rdf:Description></rdf:RDF>
