Prognostic potential of neutrophil-to-lymphocyte ratio for appendicular skeletal muscle mass reduction in males aged 70 and older DOI Creative Commons

Ying‐Jen Chen,

Chieh‐Li Yen, C H Lee

et al.

Aging, Journal Year: 2025, Volume and Issue: unknown

Published: March 6, 2025

Inflammation plays a pivotal role in the age-related decline of skeletal muscle mass, leading to sarcopenia elderly. The prevalence notably increases among males aged ≥ 70. However, it remains unclear whether inflammatory indexes are associated with reduction mass elderly population. Thirty-one 70, without severe diseases or dementia, were enrolled study. They underwent measurements, physical and hematological tests at onset study after one-year follow-up. Twenty-eight participants successfully followed for one year. Appendicular index (ASMI) decreased by 3.30 ± 2.41% 14 increased 2.66 1.61% other compared baseline levels. neutrophil-to-lymphocyte ratio (NLR) was 2.14 0.56 ASMI-decreased group 1.66 0.62 ASMI-increased group. A statistically significant negative correlation found between NLR change ASMI linear regression analyses. area under curve (AUC) predicting 0.724, an optimal sensitivity 64.3% specificity 78.6% cut-off value 1.94. emerged as potential prognostic marker males. further studies necessary assess its clinical utility.

Language: Английский

Histone β‐hydroxybutyrylation is critical in reversal of sarcopenia DOI Creative Commons
Qiquan Wang, Xinqiang Lan, Ke Hao

et al.

Aging Cell, Journal Year: 2024, Volume and Issue: 23(11)

Published: July 30, 2024

Abstract Sarcopenia, a leading cause for global disability and mortality, is an age‐related muscular disorder, characterized by accelerated muscle mass loss functional decline. It known that caloric restriction (CR), ketogenic diet or endurance exercise lessen sarcopenia elevate circulating β‐hydroxybutyrate (β‐HB) levels. Whether the elevated β‐HB essential to reversal of sarcopenia, however, remains unclear. Here we show in both Caenorhabditis elegans mouse models increase reverse myofiber atrophy improves motor functions at advanced ages. β‐HB‐induced histone lysine β‐hydroxybutyrylation (Kbhb) indispensable sarcopenia. Histone Kbhb enhances transcription genes associated with mitochondrial pathways, including oxidative phosphorylation, ATP metabolic process aerobic respiration. This ultimately leads improve integrity enhance The are validated model CR. Thus, demonstrate induces Kbhb, increases function, reverses

Language: Английский

Citations

5
Enhanced serum levels of tumor necrosis factor-α, interleukin-1β, and -6 in sarcopenia: alleviation through exercise and nutrition intervention DOI Creative Commons

Ke‐Vin Chang,

Wei‐Ting Wu, Yu‐Hsin Chen

et al.

Aging, Journal Year: 2023, Volume and Issue: 15(22), P. 13471 - 13485

Published: Nov. 29, 2023

Limited research has been conducted on the post-intervention inflammatory status in sarcopenic patients, despite previous studies revealing elevated pro-inflammatory markers. This study aimed to investigate potential elevation of specific cytokines patients and evaluate effects exercise nutritional support interventions these cytokine levels.In this post-hoc analysis a randomized controlled trial (RCT), 57 individuals with sarcopenia from RCT non-sarcopenic participants same geriatric community cohort that did not participate were enrolled. Grip strength body composition measurements recorded. Tumor necrotizing factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-15 levels assessed at baseline for both groups after 12-week intervention consisting resistive supplementation branched-chain amino acids, calcium, vitamin D3 sarcopenia.The group demonstrated significantly lower weight, mass index, grip strength, skeletal muscle index. Moreover, exhibited higher TNF-α (p=0.007), IL-1β (p<0.001), IL-6 while no significant difference was observed (p=0.345) between those without sarcopenia. Following intervention, experienced improvements index notable reduction (p=0.003), (p=0.012) (p=0.001) levels.Sarcopenic exhibit TNF-α, IL-1β, which declined nutrition interventions. However, further is necessary long-term impact levels.

Language: Английский

Citations

13
Unveiling the Intricate Dance: How Cancer Orchestrates Muscle Wasting and Sarcopenia DOI Open Access
Salvatore Lavalle, Maria Rosaria Valerio,

Edoardo Masiello

et al.

In Vivo, Journal Year: 2024, Volume and Issue: 38(4), P. 1520 - 1529

Published: Jan. 1, 2024

Sarcopenia is a prevalent and clinically significant condition, particularly among older age groups those with chronic disease. Patients cancer frequently suffer from sarcopenia progressive loss of muscle mass, strength, function. The complex interplay between its treatment, including medical therapy, radiotherapy, surgery, significantly contributes to the onset worsening sarcopenia. Cancer induces wasting through inflammatory processes, metabolic alterations, hormonal imbalance. Moreover, radiation therapies exert direct toxic effects on muscles, contributing impairment physical Loss appetite, malnutrition, inactivity further exacerbate in patients. Imaging techniques are cornerstones for diagnosis. Magnetic resonance imaging, computed tomography, dual-energy X-ray absorptiometry provide valuable insights into structure quality. Although each modality has advantages limitations, magnetic imaging produces high-resolution images provides dynamic information about Despite these challenges, addressing essential optimizing treatment outcomes improving survival rates patients cancer. This review explored factors oncologic patients, emphasizing importance early detection comprehensive management strategies.

Language: Английский

Citations

4
Network pharmacology, molecular docking, and experimental verification reveal the mechanism of Yi-Shen-Hua-Shi granules treating acute kidney injury DOI
Sheng Zhang,

Jiankui Du,

Minmin Lu

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 119320 - 119320

Published: Jan. 1, 2025

Language: Английский

Citations

0
Cyclometalated iridium(III)-lonidamine conjugates: Mitochondrial targeting and pyroptosis induction DOI

Xing-Yun Lu,

Lin-Yuan Zhu,

Zhu Hou

et al.

Journal of Inorganic Biochemistry, Journal Year: 2025, Volume and Issue: 266, P. 112852 - 112852

Published: Feb. 9, 2025

Language: Английский

Citations

0
New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses DOI Creative Commons

Xiaobo Su,

Yunjuan Sun, Aiguo Dai

et al.

APOPTOSIS, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 20, 2025

Language: Английский

Citations

0
TNF/TNFR1 Signaling Mediates DEHP-Induced Hepatocyte Pyroptosis via the GSDMD–mtROS Axis DOI
Hao Zhang,

Jia-Gen Cui,

Ming‐Shan Chen

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 25, 2025

Di(2-ethylhexyl) phthalate (DEHP), which is widely used in agricultural plastics, accumulates humans and animals through the food chain over time, resulting liver toxicity. Recent studies have reported that pyroptosis mitochondrial damage are closely related to a variety of diseases, but specific mechanism still unclear. To address this issue, vitro vivo hepatotoxicity models were established. The results demonstrated exposure DEHP caused buildup MEHP livers, altered metabolite composition, pyroptosis-like changes hepatocytes. After treatment, REDOX homeostasis was unbalanced, reactive oxygen species (mtROS) overproduced. activates mediated by TNF/TNFR1 signaling upregulates perforating protein GSDMD-N destroy membrane Above all, study elucidates potential involvement signaling-mediated confirms regulation helpful maintaining normal function.

Language: Английский

Citations

0
Zinc Alleviates Diabetic Muscle Atrophy via Modulation of the SIRT1/FoxO1 Autophagy Pathway Through GPR39 DOI Creative Commons
Xing Yu, Xiaojun Chen, Weibin Wu

et al.

Journal of Cachexia Sarcopenia and Muscle, Journal Year: 2025, Volume and Issue: 16(2)

Published: March 3, 2025

Muscle atrophy is a severe complication of diabetes, with autophagy playing critical role in its progression. Zinc has been shown to alleviate hyperglycaemia and several diabetes-related complications, but direct mediating diabetic muscle remains unclear. This study explores the potential zinc pathogenesis atrophy. In vivo, C57BL/6J mice were induced diabetes by streptozotocin (STZ) treated ZnSO₄ (25 mg/kg/day) for six weeks. Gastrocnemius muscles collected histological analysis, including transmission electron microscopy (TEM). Serum levels measured ICP-MS. Protein expression was evaluated using immunofluorescence (IF), immunohistochemistry (IHC) Western blotting (WB). Bioinformatics analysis used identify key genes associated vitro, high-glucose-induced C2C12 cell model established received ZnSO₄, rapamycin, SRT1720, TC-G-1008, or GPR39-CRISPR Cas9 intervention. Autophagy observed TEM, protein assessed IF WB. Intracellular concentrations fluorescence resonance energy transfer (FRET). atrophy, activation, upregulation SIRT1 FoxO1, along downregulation GPR39, confirmed T1D group. protected against inhibited (T1D + vs. T1D, all p < 0.0001), as evidenced increased grip strength (212.40 ± 11.08 163.90 10.95 gf), gastrocnemius index (10.67 0.44 8.80 0.72 mg/g), fibre cross-sectional area (978.20 144.00 580.20 103.30 μm2), serum (0.2335 0.0227 0.1561 0.0123 mg/L). down-regulated Atrogin-1 MuRF1, decreased formation autophagosomes (all 0.0001). RNA-seq indicated activation SIRT1/FoxO1 signalling pathway mice. LC3B, while upregulating P62 GPR39 0.05). down-regulation Both TC-G-1008 Atrogin-1, SIRT1, up-regulated inhibiting improving The beneficial anti-atrophic effects are diminished following treatment SRT1720 RAPA. Upon knockout, upregulated, downregulated. ZnSO₄-treated group remained unchanged (p > 0.05), indicating that supplementation did not affect ion entry acted through surface receptor GPR39. ZnSO4 inhibits excessive skeletal alleviates via GPR39-SIRT1/FoxO1 axis. These findings suggest may offer therapeutic strategy managing

Language: Английский

Citations

0
Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches DOI Creative Commons
Yalda Rahbar Saadat, Amin Abbasi, Seyyed Sina Hejazian

et al.

BMC Nephrology, Journal Year: 2025, Volume and Issue: 26(1)

Published: March 11, 2025

In 2008, the Society on Sarcopenia, Cachexia, and Wasting Disorders introduced a generic definition for all types of cachexia: "a complex metabolic syndrome associated with underlying illness characterized by loss muscle, or without fat loss". It is well-known that presence inflammatory burden in end-stage renal disease (ESRD) patients may lead to evolution cachexia. Since etiology cachexia chronic kidney (CKD) multifactorial, thus successful treatment must involve several concomitant measures (nutritional interventions, appetite stimulants, anti-inflammatory pharmacologic agents) provide integrated effective therapeutic modalities combat causative factors alleviate outcomes patients. Given high mortality rate cachexia, developing new are prerequisite ameliorating CKD worldwide. The present review aims discuss some strategies an update advances nutritional approaches counteract

Language: Английский

Citations

0
Cuproptosis and its potential role in musculoskeletal disease DOI Creative Commons
Zijian Xiang, Heng Mei, Honglin Wang

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 11, 2025

Cuproptosis, a recently identified form of copper-dependent cell death, arises from intracellular copper dyshomeostasis. As an essential trace element, plays critical role in bioenergetic metabolism, redox regulation, and synaptic transmission. However, excessive exerts cytotoxic effects through multiple pathways, including increased reactive oxygen species (ROS) production, apoptotic cascade activation, necrotic membrane rupture, inflammatory responses, mitochondrial dysfunction. Distinct other death mechanisms, cuproptosis is characterized by ion binding to acetylated respiratory chain proteins, leading pathogenic protein aggregation, iron-sulfur cluster depletion, cellular collapse. Emerging evidence underscores aberrant accumulation resultant proteotoxic stress as pivotal contributors the pathogenesis musculoskeletal pathologies, osteoporosis, osteoarthritis, sarcopenia, osteosarcoma, intervertebral disc degeneration, spinal cord injury, biofilm-associated orthopedic infections. Understanding spatiotemporal regulation may provide novel opportunities for advancing diagnostic therapeutic approaches medicine. This review synthesizes current insights into molecular mechanisms cuproptosis, its diseases, potential biomarker-driven interventions.

Language: Английский

Citations

0