Mitochondria play important roles in maintaining cellular homeostasis and skeletal muscle health, and damage to mitochondria can lead to a series of pathophysiological changes. Mitochondrial dysfunction can lead to skeletal muscle atrophy, and its molecular mechanism leading to skeletal muscle atrophy is complex. Understanding the pathogenesis of mitochondrial dysfunction is useful for the prevention and treatment of skeletal muscle atrophy, and finding drugs and methods to target and modulate mitochondrial function are urgent tasks in the prevention and treatment of skeletal muscle atrophy. In this review, we first discussed the roles of normal mitochondria in skeletal muscle. Importantly, we described the effect of mitochondrial dysfunction on skeletal muscle atrophy and the molecular mechanisms involved. Furthermore, the regulatory roles of different signaling pathways (AMPK-SIRT1-PGC-1α, IGF-1-PI3K-Akt-mTOR, FoxOs, JAK-STAT3, TGF-β-Smad2/3 and NF-κB pathways, etc.) and the roles of mitochondrial factors were investigated in mitochondrial dysfunction. Next, we analyzed the manifestations of mitochondrial dysfunction in muscle atrophy caused by different diseases. Finally, we summarized the preventive and therapeutic effects of targeted regulation of mitochondrial function on skeletal muscle atrophy, including drug therapy, exercise and diet, gene therapy, stem cell therapy and physical therapy. This review is of great significance for the holistic understanding of the important role of mitochondria in skeletal muscle, which is helpful for researchers to further understanding the molecular regulatory mechanism of skeletal muscle atrophy, and has an important inspiring role for the development of therapeutic strategies for muscle atrophy targeting mitochondria in the future.

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The Paleozoic construction of Pangea advanced southwestward from the Appalachian system to the Marathon fold-and-thrust belt in west Texas and progressively closed a remnant ocean basin between Laurentia and Gondwana. The resulting collisional orogen was a potential driver of Ancestral Rocky Mountain tectonism and impacted continental-scale sediment routing. New detrital zircon U-Pb geochronologic and heavy mineral provenance data from Ordovician–Pennsylvanian strata in the Marathon fold-and-thrust belt, and Permian strata in the Guadalupe Mountains of west Texas record changes in sediment provenance during the tectonic development of southwestern Laurentia and the Delaware Basin. In the Marathon fold-and-thrust belt, Ordovician rocks (Woods Hollow and Marathon Formations) record peri-Gondwanan sediment sources prior to continent collision. Syncollisional Mississippian and Pennsylvanian rocks (Tesnus, Haymond, Gaptank Formations) record contributions from distal Appalachian sources, recycled material from the active continental suture, and volcanic arc material from Gondwana. Near the Guadalupe Mountains, postcollisional Permian strata (Delaware Mountain Group) from the northern Delaware Basin margin suggest a dominantly southern catchment that was sourced from the deforming suture and Gondwanan arc. The results demonstrate that both plates and the active suture zone were sources for the siliciclastic wedge, but their proportions differed through time. These results also suggest that the delay between initial late Mississippian suturing in the Marathon region and increased mid-Permian siliciclastic deposition into the northern Delaware Basin may have been linked to a southward catchment expansion that integrated the collisional belt and southern volcanic arc into a broadly north-directed sediment dispersal system.

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