ArticleProceedings of the National Academy of Sciences of the United States of America2015
Fnip1 regulates skeletal muscle fiber type specification, fatigue resistance, and susceptibility to muscular dystrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 111 citations in OpenAlex.
- Article
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Integrated transcriptomic and proteomic analyses reveal muscle fiber-type transformation in meat rabbits.BMC genomics · 2026Article
- BRD4 directs myofiber identity and metabolic adaptation through CHD4 cooperation.Nature communications · 2026Article
- Red meat vs. white meat: A comparative analysis of histological characteristics, nutritional profiles, and health implications.Food chemistry: X · 2025Review
- Large MAF transcription factors reawaken evolutionarily dormant fast-glycolytic type IIb myofibers in human skeletal muscle.Skeletal muscle · 2025Article
- FNIP1 Deficiency: Pathophysiology and Clinical Manifestations of a Rare Syndromic Primary Immunodeficiency.Current issues in molecular biology · 2025Review
- Dnmt3a overexpression disrupts skeletal muscle homeostasis, promotes an aging-like phenotype, and reduces metabolic elasticity.iScience · 2025Article
- Aptamer-Conjugated Exosomes Ameliorate Diabetes-Induced Muscle Atrophy by Enhancing SIRT1/FoxO1/3a-Mediated Mitochondrial Function.Journal of cachexia, sarcopenia and muscle · 2025Article
- Klebsiella pneumoniae causes mammary gland damage via FNIP1-mediated mitochondrial dysfunction.Journal of animal science · 2025Article
- Action and therapeutic targets of folliculin interacting protein 1: a novel signaling mechanism in redox regulation.Frontiers in cell and developmental biology · 2025Review
- Obesity, Osteoarthritis, and Myokines: Balancing Weight Management Strategies, Myokine Regulation, and Muscle Health.Nutrients · 2024Review
- Understanding the Role of the SMN Complex Component GEMIN5 and Its Functional Relationship with Demethylase KDM6B in the Flunarizine-Mediated Neuroprotection of Motor Neuron Disease Spinal Muscular Atrophy.International journal of molecular sciences · 2024Article
- Disuse-Induced Muscle Fatigue: Facts and Assumptions.International journal of molecular sciences · 2024Review
- Effect of CB1 Receptor Deficiency on Mitochondrial Quality Control Pathways in Gastrocnemius Muscle.Biology · 2024Article
- AMPK phosphorylation of FNIP1 (S220) controls mitochondrial function and muscle fuel utilization during exercise.Science advances · 2024Article
- Molecular pathways involved in the control of contractile and metabolic properties of skeletal muscle fibers as potential therapeutic targets for Duchenne muscular dystrophy.Frontiers in physiology · 2024Review
- Alleviating effect ofFrontiers in microbiology · 2024Article
- FNIP1 abrogation promotes functional revascularization of ischemic skeletal muscle by driving macrophage recruitment.Nature communications · 2023Article
- Recent Review on Selected Xenobiotics and Their Impacts on Gut Microbiome and Metabolome.Trends in analytical chemistry : TRAC · 2023Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Mammalian skeletal muscle is broadly characterized by the presence of two distinct categories of muscle fibers called type I "red" slow twitch and type II "white" fast twitch, which display marked differences in contraction strength, metabolic strategies, and susceptibility to fatigue. The relative representation of each fiber type can have major influences on susceptibility to obesity, diabetes, and muscular dystrophies. However, the molecular factors controlling fiber type specification remain incompletely defined. In this study, we describe the control of fiber type specification and susceptibility to metabolic disease by folliculin interacting protein-1 (Fnip1). Using Fnip1 null mice, we found that loss of Fnip1 increased the representation of type I fibers characterized by increased myoglobin, slow twitch markers [myosin heavy chain 7 (MyH7), succinate dehydrogenase, troponin I 1, troponin C1, troponin T1], capillary density, and mitochondria number. Cultured Fnip1-null muscle fibers had higher oxidative capacity, and isolated Fnip1-null skeletal muscles were more resistant to postcontraction fatigue relative to WT skeletal muscles. Biochemical analyses revealed increased activation of the metabolic sensor AMP kinase (AMPK), and increased expression of the AMPK-target and transcriptional coactivator PGC1α in Fnip1 null skeletal muscle. Genetic disruption of PGC1α rescued normal levels of type I fiber markers MyH7 and myoglobin in Fnip1-null mice. Remarkably, loss of Fnip1 profoundly mitigated muscle damage in a murine model of Duchenne muscular dystrophy. These results indicate that Fnip1 controls skeletal muscle fiber type specification and warrant further study to determine whether inhibition of Fnip1 has therapeutic potential in muscular dystrophy diseases.
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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.