ArticleJournal of cachexia, sarcopenia and muscle2023
AMP-activated protein kinase inhibition in fibro-adipogenic progenitors impairs muscle regeneration and increases fibrosis.
Article in Journal of cachexia, sarcopenia and muscle, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Macrophage and fibro-adipogenic progenitor communication in skeletal muscle regeneration: tissue homeostasis and pathogenic remodeling.Journal of leukocyte biology · 2026Review
- BMPER induces the adipogenic differentiation of fibro/adipogenic progenitors and promotes intramuscular fat deposition in chickens.Journal of animal science and biotechnology · 2026Article
- Regulatory role of vitamin DScientific reports · 2025Article
- Tofogliflozin ameliorates cardiotoxin induced skeletal muscle injury and fibrosis in obesity.Scientific reports · 2025Article
- Pbk positively regulates myoblast differentiation and muscle regeneration via enhancing AMPK/ULK1 mediated myogenic autophagy.Journal of translational medicine · 2025Article
- High-Calorie Diet During Pregnancy Leads to Muscular Fibrosis and Neuromuscular Damage in Offspring Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- PdgfrαGenes & diseases · 2025Review
- Article
- Exercise and tissue fibrosis: recent advances in therapeutic potential and molecular mechanisms.Frontiers in endocrinology · 2025Review
- Aerobic exercise suppresses CCN2 secretion from senescent muscle stem cells and boosts muscle regeneration in aged mice.Journal of cachexia, sarcopenia and muscle · 2024Article
- Challenging Sarcopenia: Exploring AdipoRon in Aging Skeletal Muscle as a Healthspan-Extending Shield.Antioxidants (Basel, Switzerland) · 2024Article
- miR-27b-3p reduces muscle fibrosis during chronic skeletal muscle injury by targeting TGF-βR1/Smad pathway.Journal of orthopaedic surgery and research · 2024Article
- Fibro-adipogenic progenitors in physiological adipogenesis and intermuscular adipose tissue remodeling.Molecular aspects of medicine · 2024Review
- The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway.Biogerontology · 2024Article
- Skeletal muscle-specific inducible AMPKα1/α2 knockout mice develop muscle weakness, glycogen depletion, and fibrosis that persists during disuse atrophy.American journal of physiology. Endocrinology and metabolism · 2024Article
- Fibroadipogenic progenitors: a potential target for preventing breast muscle myopathies in broilers.Frontiers in physiology · 2024Review
- The Adiponectin Receptor Agonist, ALY688: A Promising Therapeutic for Fibrosis in the Dystrophic Muscle.Cells · 2023Article
- AMP-activated protein kinase inhibition in fibro-adipogenic progenitors impairs muscle regeneration and increases fibrosis.Journal of cachexia, sarcopenia and muscle · 2023Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundFollowing muscle injury, fibro-adipogenic progenitors (FAPs) are rapidly activated and undergo apoptosis at the resolution stage, which is required for proper muscle regeneration. When excessive FAPs remain, it contributes to fibrotic and fatty infiltration, impairing muscle recovery. Mechanisms controlling FAP apoptosis remain poorly defined. We hypothesized that AMP-activated protein kinase (AMPK) in FAPs mediates their apoptosis during the muscle regeneration.
methodsTo test, AMPKα1
resultsWe found that AMPKα1 deletion in FAPs enhanced p65 translocation to the nuclei by 110% (n = 3; P < 0.01). AMPKα1 knockout group had a higher gene expression of MMP-9 (matrix metalloproteinase-9) by 470% (n = 3; P < 0.05) and protein level by 39% (n = 3; P < 0.05). Loss of AMPKα1 up-regulated the active TGF-β1 (transforming growth factor-β1) levels by 21% (n = 3; P < 0.05). TGF-β promoted apoptotic resistance, because AMPKα1-deficient group had 36% lower cleaved Caspase 3 (cCAS3) content (n = 3; P < 0.05). Fibrotic differentiation of FAPs was promoted, with increased collagen protein level by 54% (n = 3; P < 0.05). Moreover, obesity decreased phosphorylation of AMPK by 54% (n = 3; P < 0.05), which decreased cCAS3 in FAPs by 44% (n = 3; P < 0.05) and elevated collagen accumulation (52%; n = 3; P < 0.05) during muscle regeneration.
conclusionsThese data suggest that AMPK is a key mediator of FAPs apoptosis, and its inhibition due to obesity results in fibrosis of regenerated muscle.
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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.