Skeletal muscle aging is a complex biological process that involves coordinated changes in multiple cell types. Recent breakthroughs in single-cell sequencing technology have provided new perspectives regarding this process. Here, we systematically summarize current progress in single-cell technology with respect to skeletal muscle aging. We focused on specific molecular characteristics and interaction networks of muscle fiber, satellite and immune cells during aging. Aging skeletal muscles develop cellular heterogeneity such as a decline in stem cell function, formation of a chronic inflammatory microenvironment, and remodeling the extracellular matrix. We integrated multi-omics data to identify potential intervention targets and explored precise anti-aging strategies using single-cell data. Although this field has significantly progressed, persistent challenges include technical methods, data integration, and clinical translation. Future studies are needed to optimize single-cell analysis techniques, deepen understanding of cell interaction mechanisms, and promote the translation of related findings into clinical applications. These will provide vital references for understanding the molecular basis of muscle aging and developing new intervention methods.
Yanteng Wang, Yichen Yang, W. Guan et al.· Ageing Research Reviews· 0 citations
Background
Few studies have investigated the association between cardiovascular health (CVH) and thyroid dysfunction, and the modifying role of depression or anxiety remains unclear.
Methods
This longitudinal study included 360,332 UK Biobank participants without thyroid disease at baseline and with complete CVH scores. We examined the associations between CVH and the risks of hyperthyroidism and hypothyroidism using Cox proportional hazards regression models, quantified the relative contributions of CVH components using weighted quantile sum regression, and evaluated the mediating role of inflammatory markers. Furthermore, we investigated the modifying effects of depression and anxiety on these associations. A multi-state model was used to explore disease trajectories.
Results
During a median follow-up of 12.53 years, 1,533 and 7,542 participants developed hyperthyroidism and hypothyroidism, respectively. After multivariable adjustment, each 5-point increase in CVH score was associated with a 7% (95% confidence interval [CI], 4% to 9%) lower risk of hyperthyroidism and an 8% (95% CI, 7% to 9%) lower risk of hypothyroidism. A high CVH score was associated with a 50% (95% CI, 37% to 60%) lower risk of hyperthyroidism and a 45% (95% CI, 38% to 50%) lower risk of hypothyroidism. Among the CVH components, obesity and tobacco exposure contributed most to disease risk. Inflammatory markers partially mediated these associations. Depression and anxiety modified the association between CVH and hypothyroidism, and CVH showed a protective effect across the disease trajectories.
Conclusion
Maintaining favorable CVH was associated with a lower risk of thyroid dysfunction, particularly among individuals with good mental health.
Jilong Bai, Rui Ren, Panting Wei et al.· Endocrinology and Metabolism· 0 citations
ABSTRACT Aim Skeletal muscle atrophy is tightly associated with maladaptive alterations in mitochondrial function and morphology. Itchy E3 ubiquitin‐protein ligase (ITCH) modulates mitochondria, and thrombospondin 1 (THBS1) positively regulates muscle atrophy, but their roles in muscle atrophy are unclear. Methods A muscle atrophy model was established in C57BL/6 mice via daily intraperitoneal injection of dexamethasone (Dex, 20 mg/kg). ITCH overexpression in skeletal muscle was achieved by adeno‐associated virus serotype 9 injection. C2C12 cells were treated with 50 μM Dex to mimic in vitro muscle atrophy. Skeletal muscle atrophy in mice was evaluated using hematoxylin–eosin staining and immunofluorescence staining. Mitochondrial damage was assessed via transmission electron microscopy, succinate dehydrogenase staining, and JC‐1 staining. Immunoprecipitation‐liquid chromatography/mass spectrometry, molecular docking, and co‐immunoprecipitation were used to investigate the interaction between ITCH and THBS1. Phosphoproteomics analysis was performed to detect the THBS1 downstream proteins. Results Dex treatment downregulated ITCH expression in skeletal muscle. ITCH overexpression increased body weight, muscle mass, and muscle strength, downregulated the expression of atrophy‐related genes (Atrogin‐1, Mstn, MuRF‐1), and promoted mitochondrial biogenesis. The results of the C2C12 cells were consistent with those obtained in vivo. Proteomic profiling and Co‐IP confirmed ITCH–THBS1 interaction and subsequent THBS1 ubiquitination. THBS1 knockdown reduced the expression of Atrogin‐1 and MuRF‐1 and inhibited the phosphorylation of JUN and Map3k7, whereas THBS1 overexpression reversed the ITCH‐mediated improvement in mitochondrial biogenesis. Conclusion ITCH enhances mitochondrial biogenesis and mitigates Dex‐induced muscle atrophy by promoting the ubiquitin‐dependent degradation of THBS1 and subsequent inhibition of downstream JUN/Map3k7 phosphorylation.
Wan Yu, Yanteng Wang, Na Li et al.· Acta Physiologica· 0 citations
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