ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR222/006/SRR22240306/SRR22240306_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR222/005/SRR22240305/SRR22240305_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR222/004/SRR22240304/SRR22240304_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR222/006/SRR22240306/SRR22240306_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR222/004/SRR22240304/SRR22240304_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR222/005/SRR22240305/SRR22240305_2.fastq.gzprimaryOK200GenomicsSichuan University West China Hospitalhttps://www.ebi.ac.uk/ena/browser/view/PRJNA899596Sarcopenia is known as age-related muscle atrophy that affects more than a quarter of the elderly population worldwide. It is characterized by progressive decline in muscle mass, strength and performance, which deteriorated life quality and increased mortality eventually. Up to date, clinical treatments in sarcopenia are limited to rehabilitative interventions and dietary supplements only, without any effective therapeutics. In this study, tetrahedral framework nucleic acids (tFNAs) were utilized to treat sarcopenia both in vitro and in vivo. tFNAs participated in the maintenance of mitochondria energy metabolism by regulating mitochondrial outer membrane permeabilization and the preservation of mitochondrial ultra-structures by inhibiting excessive mitochondrial fission. tFNAs also down-regulated cell apoptosis via BIM/BclxL mitochondria-regulated pathway, which is closely related to the pathogenic mechanism of sarcopenia. Furthermore, tFNAs altered the size and arrangement of muscle fibers to enhance muscle stiffness in sarcopenia mouse model. Altogether, these findings proved that tFNAs were effective in ameliorating age-related muscle atrophy and hence could be a promising treatment option for sarcopenia in the future.ENANeurogenic Muscular, cellular suicide, cell suicide, Caspase-Dependent Apoptosis, acide nucleique, caspase-dependent programmed cell death, apoptotic cell death, Muscle hypotrophy, Neurogenic muscle atrophy, Caspase Dependent Apoptosis, type I programmed cell death, apoptotic programmed cell death, Neurogenic, Muscle, Mitochondrial Contractions, Neurotrophic, Amyotrophy involving the extremities, Neurotrophic Muscular, activation of apoptosis, Muscular Atrophies, sarcopenias, Contractions, especially in the lower limbs, acides nucleiques, signaling (initiator) caspase activity, induction of apoptosis, Extrinsic Pathway Apoptoses, Neurotrophic Muscular Atrophy, nucleic acids, Intrinsic Pathway, Programmed, Nucleic Acid, neurogenic, Neurotrophic Muscular Atrophies, Programmed Cell Death, Extrinsic Pathway Apoptosis, Neurogenic Muscular Atrophies, Mitochondrion, NA, Type I, Caspase-Dependent, Atrophies, apoptosis signaling, Acid, Muscle Atrophies, Mitochondrial, Muscular Atrophy, Muscle wasting, Neurogenic Muscular Atrophy, Nukleinsaeure, apoptosis, Neurogenic muscular atrophy, Contraction, Atrophy, acido nucleico, Cell Death, apoptosis activator activity, Nucleic, Mitochondrial Contraction, Classic Apoptoses, Intrinsic Pathway Apoptoses, Muscle atrophy, Intrinsic Pathway Apoptosis, Muscle degeneration, Amyotrophy, mitochondria, acidos nucleicos, induction of apoptosis by p53, Classic, Classic Apoptosis, apoptotic program, Nukleinsaeuren, execution phase of apoptotic process, Muscular atrophy, Classical Apoptosis, muscle wasting, Extrinsic Pathway, commitment to apoptosis, Acids, programmed cell death by apoptosis, Classical, Muscular, Muscle Atrophy, Apoptoses, Sarcopenias., ApoptosisfalseTetrahedral framework nucleic acids inhibit muscular mitochondria-mediated apoptosis and ameliorate muscle atrophy in Sarcopenia2023-11-182023-11-18PRJNA899596