BACKGROUND

Sarcopenia is highly prevalent in patients with liver cirrhosis and contributes to decreased quality of life, increased morbidity, and mortality. The role of myostatin in cirrhosis-related sarcopenia remains controversial but may represent a potential therapeutic target.

This study aimed to investigate the association between serum myostatin levels and sarcopenia in patients with liver cirrhosis.

A cross-sectional study was conducted with 80 patients diagnosed with liver cirrhosis at Prof. Dr. I.G.N.G. Ngoerah General Hospital, Denpasar, Bali, Indonesia. Serum myostatin levels (ng/L) were measured using an ELISA technique. Sarcopenia was diagnosed based on the 2019 Asian Working Group for Sarcopenia (AWGS) consensus. Elevated myostatin levels were defined as values above the median. Bivariate and multivariate analyses were performed to assess associations between myostatin, cirrhosis severity, and sarcopenia.

The severity of cirrhosis (CTP B and C) was associated with elevated myostatin levels (PR = 2.046; 95% CI: 1.310–3.193; p = 0.002). Bivariate analysis demonstrated that elevated myostatin (PR = 2.178; 95% CI: 1.370–3.461; p < 0.001), CTP B and C (PR = 1.818; 95% CI: 1.223–2.701; p = 0.004), ascites (PR = 1.606; 95% CI: 1.110–2.324; p = 0.034), and malnutrition (PR = 1.806; 95% CI: 1.242–2.626; p = 0.004) were associated with sarcopenia. In multivariate analysis, only elevated serum myostatin remained significantly associated with sarcopenia (AOR = 4.273; 95% CI: 1.557–11.724; p = 0.005).

Elevated serum myostatin levels are strongly associated with sarcopenia in patients with liver cirrhosis. Cirrhosis severity is also linked to higher myostatin levels, suggesting a potential role for myostatin-targeted interventions in sarcopenia management.

Abstract Background: Sarcopenia and frailty are common geriatric syndromes that may contribute to mild cognitive impairment (MCI). Evidence regarding the independent roles of individual sarcopenia components and frailty in MCI remains limited in low- and middle-income countries. This study evaluated the association between sarcopenia components, frailty, and MCI among older adults in Indonesia. Methods: An ambispective cohort study was conducted among adults aged ≥60 years attending the Geriatric Outpatient Clinic of Dr. Cipto Mangunkusumo National General Hospital, Jakarta. Sarcopenia components were assessed using SARC-Calf (low muscle mass indicator), handgrip strength, and the five-times sit-to-stand test. Frailty was evaluated using the FRAIL scale. Cognitive function was assessed using the Rapid Cognitive Screening. Multivariate log-binomial or Poisson regression with robust variance was used to estimate adjusted risk ratios (RRs) for MCI. Results: A total of 121 participants (median age 74 years; 68.6% female) were included, with an MCI prevalence of 21.5%. After adjustment for confounders, low muscle mass indicator (RR 2.206; 95% CI 1.045–4.652) and low muscle strength (RR 3.006; 95% CI 1.202–7.517) were independently associated with MCI. Low physical performance (RR 1.773; 95% CI 0.796–3.773) and frailty (RR 1.086; 95% CI 0.377–3.134) were not significantly associated with MCI. Conclusion: Low muscle mass indicators and reduced muscle strength were independently associated with MCI, supporting the integration of simple sarcopenia screening tools into routine geriatric cognitive assessment.
sarcopenia ; frailty ; mild cognitive impairment ; rapid cognitive screening

Stroke-associated sarcopenia is a serious post-stroke complication that can have a significant impact on patient’s functional recovery. However， currently available assessment tools for sarcopenia require specialized equipment and personnel， which are difficult to access in resource-limited settings. This article presents the role of biomarkers as an objective method in the pathogenesis， prevention， diagnosis， and prognostic assessment of stroke-associated sarcopenia， with the focus on neuromuscular， inflammatory， metabolic， and nutritional indicators.
Stroke ; Sarcopenia ; Biomarkers

Objective To investigate the incidence rate of sarcopenia and related risk factors in patients with stroke. Methods A retrospective analysis was performed for the patients with stroke who were admitted to the stroke center of a grade A tertiary hospital in Changchun， China， from March 2023 to June 2024. The method of bioelectrical impedance was used to perform body composition analysis for all patients on day（7.0±1.0）after admission， and the incidence rate of stroke-related sarcopenia was analyzed. A binary logistic regression analysis was used to investigate the risk factors for stroke-related sarcopenia. Results A total of 666 patients were included in the study， among whom 150（22.5%） developed sarcopenia （95%CI 0.193‒ 0.257）. Low body mass index， low phase angle， low triglyceride， advanced age， and low Barthel index were risk factors for the early onset of sarcopenia in patients with stroke. Conclusion There is a relatively high incidence rate of sarcopenia in stroke patients， with complex influencing factors. Medical staff should pay more attention to the elderly stroke patients， as well as those patients with emaciation， low phase angle， low triglyceride， and limited activities of daily living. Early nutritional supplementation and functional exercise can help to prevent the onset of stroke-related sarcopenia.
Stroke ; Sarcopenia

Aging is typically associated with decreased musculoskeletal function, leading to reduced mobility and increased frailty. As a hallmark of aging, cellular senescence plays a crucial role in various age-related musculoskeletal diseases, including osteoporosis, osteoarthritis, intervertebral disc degeneration, and sarcopenia. The detrimental effects of senescence are primarily due to impaired regenerative capacity of stem cells and the pro-inflammatory environment created by accumulated senescent cells. The secreted senescence-associated secretory phenotype (SASP) can induce senescence in neighboring cells, further amplifying senescent signals. Although the removal of senescent cells and the suppression of SASP factors have shown promise in alleviating disease progression and restoring musculoskeletal health in mouse models, clinical trials have yet to demonstrate significant efficacy. This review summarizes the mechanisms of cellular senescence in age-related musculoskeletal diseases and discusses potential therapeutic strategies targeting cellular senescence.
Humans ; Cellular Senescence/physiology* ; Musculoskeletal Diseases/pathology* ; Aging/pathology* ; Animals ; Senescence-Associated Secretory Phenotype/physiology* ; Sarcopenia ; Osteoporosis

OBJECTIVE: To compare the effects of piriformis muscle release versus preservation in total hip arthroplasty (THA) via supercapsular percutaneously-assisted total hip (SuperPATH) approach on muscle injury. METHODS: Forty-nine patients undergoing initial THA via SuperPATH approach between June 2022 and June 2023 were randomly divided into two groups, with 24 patients in trial group and 25 patients in control group. The trial group received piriformis muscle release intraoperatively, whereas the control group underwent muscle preservation. There was no significant difference in baseline data such as gender, age, body mass index, disease type, American Society of Anesthesiologists (ASA) grading, and preoperative muscle infiltration, muscle atrophy, muscle injury serological indicators, Harris score, etc. ( P>0.05). The incision length, operation time, intraoperative blood loss, total blood loss, hospital stay, preoperative and postoperative 1-day muscle injury serological indicators [including creatine kinase (CK) and lactic dehydrogenase (LDH)], and incidence of complications between two groups were recorded. Harris score was used to evaluate the recovery of hip joint function. MRI was used to evaluate the extent of hip muscle injuries (gluteus minimus, gluteus medius, piriformis, obturator internus, quadratus femoris), including tendon integrity, degree of muscle fat infiltration, and degree of muscle atrophy preoperative and 1 year postoperatively. RESULTS: The operation time, intraoperative blood loss, and total blood loss in the trial group were significantly shorter than those in the control group ( P<0.05). There was no significant difference in the incision length and length of hospital stay between the two groups ( P>0.05). Both groups showed a significant increase in serum CK and LDH levels on postoperative day 1 compared to preoperative levels ( P<0.05), but there was no significant difference between the two groups ( P>0.05). All patients were followed up, the follow-up time for the trial group and the control group was (14.8±2.8) and (15.1±3.0) months, respectively, with no significant difference ( t=-0.400, P=0.691). Incisions healed by first intention in both groups, with 1 case in the trial group and 2 cases in the control group experiencing venous thrombosis in the calf muscle space. There was no complication such as deep vein thrombosis, pulmonary embolism, hip dislocation, prosthesis loosening, or periprosthetic infection in the lower limbs. There was no significant difference in the incidence of complications between the two groups ( P>0.05). At 1 year after operation, both groups of patients showed a significant increase in Harris scores compared to preoperative levels ( P<0.05), but there was no significant difference between the two groups ( P>0.05). Compared with preoperative results, both groups showed significant fat infiltration in the piriformis and obturator muscles at 1 year after operation ( P<0.05), while there was no significant fat infiltration in the gluteus minimus, gluteus medius, and quadratus femoris muscles ( P>0.05). At 1 year after operation, except for the higher incidence of piriformis muscle fat infiltration in the control group compared to the trial group ( P<0.05), there was no significant difference in the incidence of other muscle infiltrations between the two groups ( P>0.05). At 1 year after operation, both groups of piriformis and obturator muscles showed significant muscle atrophy compared to preoperative levels ( P<0.05). The gluteus minimus and gluteus medius showed mild atrophy compared to preoperative levels, while the maximum transverse diameter of the quadriceps muscle slightly increased, but the differences were not significant ( P>0.05). There was no significant difference in the maximum cross-sectional diameter or cross-sectional area changes of each muscle between the two groups ( P>0.05). At 1 year after operation, the continuity of the gluteus medius and quadratus femoris muscles in both groups was intact. Both groups had some patients with incomplete continuity of the piriformis muscle, obturator internus, and gluteus minimus, but the difference was not significant ( P>0.05). CONCLUSION The SuperPATH approach THA may cause injury to the piriformis, gluteus minimus, and obturator internus. The piriformis muscle release does not increase muscle injury, but it can shorten the operation time and reduce bleeding.
Humans ; Arthroplasty, Replacement, Hip/adverse effects* ; Male ; Female ; Muscle, Skeletal/surgery* ; Middle Aged ; Aged ; Postoperative Complications/epidemiology* ; Adult ; Operative Time ; Muscular Atrophy ; Creatine Kinase/blood* ; Length of Stay ; Treatment Outcome

OBJECTIVE: To assess the impacts of electroacupuncture (EA) on the gait, oxidative stress, inflammatory reaction, and protein degradation in the rats of denervated skeletal muscle atrophy, and explore the potential mechanism of EA for alleviating denervated skeletal muscle atrophy. METHODS: Forty male SD rats, 8 weeks old, were randomly assigned to a sham-surgery group, a model group, an EA group, and a p38 MAPK inhibitor group, with 10 rats in each group. The right sciatic nerve was transected to establish a rat model of denervated skeletal muscle atrophy in the model group, the EA group and the p38 MAPK inhibitor group. In the sham-surgery group, the nerve was exposed without transection. One day after successful modeling, the rats in the EA group received EA at "Huantiao" (GB30) and "Zusanli" (ST36) on the right side, using a continuous wave with a frequency of 2 Hz and current intensity of 1 mA, for 15 min in each session, EA was delivered once a day, 6 times a week. In the p38 MAPK inhibitor group, the rats received the intraperitoneal injection with SB203580 (5 mg/kg), once a day, 6 times a week. The intervention was composed of 3 weeks in each group. After the intervention completion, the CatWalk XT 10.6 animal gait analysis system was used to record the gait parameters of rats. The wet weight ratio of the gastrocnemius muscle was calculated after the sample collected. Using HE staining, the fiber morphology and cross-sectional area of the gastrocnemius muscle were observed; ELISA was employed to measure the content of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α in the gastrocnemius muscle; the biochemical hydroxyamine method was adopted to detect the content of superoxide dismutase (SOD) and malondialdehyde (MDA) in the gastrocnemius muscle; with immunohistochemistry and Western blot used, the expression of p38 mitogen-activated protein kinase (p38 MAPK), phosphorylated (p)-p38 MAPK, muscle atrophy F-box gene (Atrogin-1), muscle RING finger 1 (Murf-1), nuclear factor E2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) was detected in the gastrocnemius muscle. RESULTS: Compared to the sham-surgery group, in the model group, the standing duration, the swing time and the step cycle were increased (P<0.001), the footprint area of the maximum contact time, the print area, the average intensity of the maximum contact time, the average intensity, the swing speed, and the step length were decreased (P<0.001); the wet weight ratio of gastrocnemius muscle and fiber cross-sectional area were reduced (P<0.001); the content of IL-6, IL-1β, TNF-α and MDA in gastrocnemius muscle elevated (P<0.001), and that of SOD reduced (P<0.001); the positive and protein expression of p-p38 MAPK, Atrogin-1 and Murf-1 elevated (P<0.001) and that of Nrf2 and HO-1 dropped (P<0.001). When compared with the model group, in the EA group and the p38 MAPK inhibitor group, the standing duration, the swing time and the step cycle decreased (P<0.01), the footprint area of the maximum contact time, the print area, the average intensity of the maximum contact time, the average intensity, the swing speed, and the step length increased (P<0.01); the wet weight ratio of gastrocnemius muscle and fiber cross-sectional area were improved (P<0.01, P<0.05); the content of IL-6, IL-1β, TNF-α and MDA in gastrocnemius muscle dropped (P<0.05, P<0.01), and that of SOD elevated (P<0.01, P<0.05); the positive and protein expression of p-p38 MAPK, Atrogin-1 and Murf-1 dropped (P<0.01, P<0.05) and that of Nrf2 and HO-1 increased (P<0.01, P<0.05). CONCLUSION Electroacupuncture may alleviate skeletal muscle atrophy in denervated skeletal muscle atrophy rats by mediating the p38 MAPK activity, thereby suppressing oxidative stress, inflammatory reaction, and protein degradation.
Animals ; Electroacupuncture ; Male ; Rats ; p38 Mitogen-Activated Protein Kinases/genetics* ; Rats, Sprague-Dawley ; Muscular Atrophy/metabolism* ; Muscle, Skeletal/metabolism* ; Humans ; Signal Transduction ; Superoxide Dismutase/genetics* ; Tumor Necrosis Factor-alpha/genetics* ; Oxidative Stress ; MAP Kinase Signaling System ; Acupuncture Points

INTRODUCTION: The diagnosis of sarcopenia relies on key indicators such as handgrip strength, walking speed and muscle mass. Developing a composite index that integrates these measures could enhance clinical evaluation in older adults. This study aimed to standardise and combine these metrics to establish a z score for the sarcopenia composite index (ZoSCI) tailored for the ageing population. Additionally, we explore the risk factors associated with ZoSCI to provide insights into early prevention and intervention strategies. METHOD: This retrospective study analysed data between January 2017 and December 2021 from an elderly health programme in Taiwan, applying the Asian Working Group for Sarcopenia criteria to assess sarcopenia. ZoSCI was developed by standardising handgrip strength, walking speed and muscle mass into z scores and integrating them into a composite index. Receiver operating characteristic (ROC) curve analysis was used to determine optimal cut-off values, and multiple regression analysis identified factors influencing ZoSCI. RESULTS: Among the 5047 participants, the prevalence of sarcopenia was 3.7%, lower than the reported global prevalence of 3.9-15.4%. ROC curve analysis established optimal cut-off points for distinguishing sarcopenia in ZoSCI: -1.85 (sensitivity 0.91, specificity 0.88) for males and -1.97 (sensitivity 0.93, specificity 0.88) for females. Factors associated with lower ZoSCI included advanced age, lower education levels, reduced exercise frequency, lower body mass index and creatinine levels. CONCLUSION This study introduces ZoSCI, a new compo-site quantitative indicator for identifying sarcopenia in older adults. The findings highlight specific risk factors that can inform early intervention. Future studies should validate ZoSCI globally, with international collaborations to ensure broader applicability.
Humans ; Sarcopenia/physiopathology* ; Male ; Aged ; Female ; Retrospective Studies ; Hand Strength ; Taiwan/epidemiology* ; ROC Curve ; Aged, 80 and over ; Risk Factors ; Walking Speed ; Geriatric Assessment/methods* ; Prevalence ; Muscle, Skeletal ; Middle Aged

This study aims to explore the role and mechanism of CXC chemokine receptor 3 (CXCR3) in cisplatin-induced skeletal muscle atrophy. Wild-type mice were divided into two groups: cisplatin group and control group (treated by normal saline). The results showed that, compared to the control group, the expression levels of CXCR3 mRNA and protein were significantly up-regulated in the skeletal muscle of the cisplatin group, suggesting that CXCR3 may play an important role in the model of cisplatin-induced skeletal muscle atrophy. To further investigate its role and potential mechanisms, CXCR3 knockout mice and wild-type mice were treated with cisplatin to induce skeletal muscle atrophy. The results revealed that CXCR3 knockout not only failed to alleviate cisplatin-induced skeletal muscle atrophy, but also further reduced body weight, skeletal muscle mass, and muscle fiber cross-sectional area. Further analysis showed that, in the cisplatin-induced muscle atrophy model, CXCR3 knockout significantly up-regulated the expression levels of E3 ubiquitin ligases in skeletal muscle and down-regulated the expression levels of myogenic regulatory factors. To explore the molecular mechanism by which CXCR3 gene deletion exacerbated cisplatin-induced skeletal muscle atrophy, transcriptomic sequencing was performed on the atrophied skeletal muscles of wild-type and CXCR3 knockout mice. The results showed that, compared to wild-type mice, 14 genes were significantly up-regulated and 12 genes were significantly down-regulated in the skeletal muscle of CXCR3 knockout mice. Gene set enrichment analysis (GSEA) revealed a significant enrichment of genes related to fatty acid β-oxidation. Quantitative real-time PCR validation results were consistent with the transcriptomic sequencing results. These findings suggest that CXCR3 may counteract cisplatin-induced skeletal muscle atrophy by up-regulating E3 ubiquitin ligases, down-regulating myogenic regulatory factors, and enhancing the recruitment of fatty acid β-oxidation-related genes.
Animals ; Cisplatin/adverse effects* ; Muscular Atrophy/physiopathology* ; Mice ; Receptors, CXCR3/metabolism* ; Ubiquitin-Protein Ligases/metabolism* ; Mice, Knockout ; Oxidation-Reduction ; Fatty Acids/metabolism* ; Muscle, Skeletal/metabolism* ; Mice, Inbred C57BL ; Male

The increasing prevalence of aging has led to a rising incidence of comorbidity of sarcopenia and obesity, posing significant burdens on socioeconomic and public health. Current research has systematically explored the pathogenesis of each condition; however, the mechanisms underlying their comorbidity remain unclear. This study reviews the current literature on sarcopenia and obesity in the aging population, focusing on their shared biological mechanisms, which include loss of autophagy, abnormal macrophage function, mitochondrial dysfunction, and reduced sex hormone secretion. It also identifies metabolic mechanisms such as insulin resistance, vitamin D metabolism abnormalities, dysregulation of iron metabolism, decreased levels of nicotinamide adenine dinucleotide, and gut microbiota imbalances. Additionally, this study also explores the important role of genetic factors, such as alleles and microRNAs, in the co-occurrence of sarcopenia and obesity. A better understanding of these mechanisms is vital for developing clinical interventions and preventive strategies.
Humans ; Sarcopenia/physiopathology* ; Obesity/physiopathology* ; Aging/physiology* ; Autophagy/physiology* ; Insulin Resistance ; Comorbidity ; Vitamin D/metabolism* ; Gonadal Steroid Hormones/metabolism* ; Gastrointestinal Microbiome ; Mitochondria ; MicroRNAs