Inhibiting Myostatin Expression by the Antisense Oligonucleotides Improves Muscle Wasting in a Chronic Kidney Disease Mouse Model DOI Open Access

Afsana Akhter,

Abdullah Md. Sheikh, Jun Yoshino

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(7), P. 3098 - 3098

Published: March 27, 2025

Sarcopenia, a serious consequence of chronic kidney disease (CKD), is driven by elevated myostatin (MSTN), key inhibitor muscle growth. This study explored the potential an MSTN-specific antisense oligonucleotide (ASO) in reversing CKD-induced wasting mouse model. Thirty-two male C57BL/6J mice were randomly assigned to non-CKD group (n = 8, regular diet) and CKD 24, adenine diet). was induced using 0.2% adenine-supplemented diet for 4 weeks. Following this, sub-grouped into (saline, n 8), + Low-Dose ASO (25 mg/kg ASO, High-Dose (50 8). administered via subcutaneous injections 8 Muscle mass, treadmill performance, grip strength, fiber morphology assessed alongside qPCR Western blot analysis MSTN, atrogin-1, MuRF-1 expression. therapy significantly enhanced mass function enlarged fibers while effectively downregulating degradation markers. These improvements occurred without compromising renal function, as confirmed BUN, creatinine, weight, histological analysis. first demonstrate efficacy mitigating sarcopenia, offering promising targeted gene with significant clinical implications improving nutritional status physical performance CKD.

Language: Английский

Inhibiting Myostatin Expression by the Antisense Oligonucleotides Improves Muscle Wasting in a Chronic Kidney Disease Mouse Model DOI Open Access

Afsana Akhter,

Abdullah Md. Sheikh, Jun Yoshino

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(7), P. 3098 - 3098

Published: March 27, 2025

Sarcopenia, a serious consequence of chronic kidney disease (CKD), is driven by elevated myostatin (MSTN), key inhibitor muscle growth. This study explored the potential an MSTN-specific antisense oligonucleotide (ASO) in reversing CKD-induced wasting mouse model. Thirty-two male C57BL/6J mice were randomly assigned to non-CKD group (n = 8, regular diet) and CKD 24, adenine diet). was induced using 0.2% adenine-supplemented diet for 4 weeks. Following this, sub-grouped into (saline, n 8), + Low-Dose ASO (25 mg/kg ASO, High-Dose (50 8). administered via subcutaneous injections 8 Muscle mass, treadmill performance, grip strength, fiber morphology assessed alongside qPCR Western blot analysis MSTN, atrogin-1, MuRF-1 expression. therapy significantly enhanced mass function enlarged fibers while effectively downregulating degradation markers. These improvements occurred without compromising renal function, as confirmed BUN, creatinine, weight, histological analysis. first demonstrate efficacy mitigating sarcopenia, offering promising targeted gene with significant clinical implications improving nutritional status physical performance CKD.

Language: Английский

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