Ask about this productRelated genes to: GDF8 protein
- Gene:
- MSTN NIH gene
- Name:
- myostatin
- Previous symbol:
- GDF8
- Synonyms:
- -
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-12
- Date modifiied:
- 2019-04-23
Related products to: GDF8 protein
Related articles to: GDF8 protein
- Exercise can regulate the physiological functions of the body by inducing the secretion of myokines, which are bioactive factors mainly secreted by muscle cells. This review classifies myokines based on their functional characteristics, including metabolic regulation (such as myostatin, interleukin-6), neuroregulation (brain-derived neurotrophic factor), cell proliferation/differentiation regulation (myogenic proteins), immune regulation (tumor necrosis factor- alpha), and factors involved in angiogenesis and extracellular matrix remodeling (such as connective tissue growth factor).Cancer, as a consuming disease, often accompanies muscle atrophy and depletion in its advanced stage, thereby affecting the normal secretion of myokines. Increasing research evidence indicates that myokines play a dual regulatory role in the occurrence and development of cancer. Some myokines (such as interleukin-6, tumor necrosis factor- alpha) have environment-dependent functions and can exhibit pro-cancer or anti-cancer effects depending on the microenvironment; while factors such as myostatin show stable anti-tumor potential by regulating key molecular pathways such as the PI3K/AKT pathway, epithelial-mesenchymal transition, and HIF-1α. It is worth noting that muscle cell factors can indirectly influence the disease outcome of cancer by regulating key cells and structures in the tumor microenvironment (such as tumor-associated macrophages, regulatory T cells, and cancer-associated fibroblasts), as well as by participating in the angiogenesis process. At the clinical application level, muscle cell factors are expected to become potential biomarkers for cancer diagnosis and prognosis assessment (such as elevated irisin levels in patients with renal cancer and elevated interleukin-6 levels in patients with bile duct cancer). They also have great potential as therapeutic targets. For example, MSTN inhibitors can effectively alleviate cancer cachexia symptoms, and the combination of anti-interleukin-6 treatment with immune checkpoint blockade therapy can produce a significant synergistic therapeutic effect. This review systematically summarizes the latest research progress on the molecular interaction mechanisms mediated by myokines in cancer, emphasizing their potential for translational applications in precision oncology. Myokines not only regulate the physiological functions of the musculoskeletal system, but also have a close association with the occurrence and development of cancer. The intrinsic connection between myokines and muscle atrophy as well as cancer-related cachexia still requires further in-depth exploration. As emerging biomarkers, myokines can be combined with various diagnostic and therapeutic techniques, which is expected to further improve the survival rate of cancer patients, protect muscle function, and also provide new research ideas for exploring the interrelationship between muscles and cancer and the pathogenesis of related muscle diseases. - Source: PubMed
Publication date: 2026/04/21
Zhang HuizheFu DongjingYue MeijingCheng FenJiang YingZhao JuanWang WenjuanDeng ShuqingTian DanJin GaowaLi Quanfu - Sarcopenia is a frequent and clinically relevant condition in patients with pancreatic neoplasm, contributing to poor prognosis, reduced therapeutic tolerance, and increased mortality. The identification of reliable circulating biomarkers, alongside imaging-based muscle assessment, may improve early detection and risk stratification. This randomized prospective study included 61 patients, of whom 36 had pancreatic neoplasm associated with sarcopenia and 25 served as controls. Serum levels of osteonectin (SPARC), C-terminal agrin fragment (CAF), procollagen type III N-terminal peptide (P3NP), myostatin (MSTN), and insulin-like growth factor-1 (IGF-1) were measured using ELISA. Skeletal muscle index (SMI) and psoas muscle index (PMI) were assessed using CT at the L3 level. Patients with pancreatic neoplasm and sarcopenia showed significantly altered biomarker profiles compared to controls. Osteonectin (median 936.4 vs. 539.9, p 0.001), CAF (2135.9 vs. 1165.5, p 0.001), P3NP (8.01 vs. 5.34, p 0.001), myostatin (47.71 vs. 7.85, p 0.001), and IGF-1 (142 vs. 106.7, p 0.001) were all elevated. The highest biomarker levels were consistently observed in the pancreatic neoplasm group compared to other disease groups. Additionally, 100% of patients with pancreatic neoplasm exhibited reduced SMI, confirming the high prevalence of sarcopenia. Biomarker levels were not significantly influenced by tumor location. The combined use of circulating biomarkers and CT-derived muscle indices provides a clinically relevant approach for identifying sarcopenia in pancreatic cancer. - Source: PubMed
Gherghescu Costel-GeorgeBaz Radu AndreiDina ConstantinDumitru EugenCozaru Georgeta CameliaManea MihaelaPopescu IoanaGrigorescu Ana-MariaPopescu StereDumitru Andrei - This study aimed to evaluate the effects of dietary supplementation with the hexane fraction of Ulva fasciata extract (UH) on growth performance, immune responses, and antioxidant status in Nile tilapia (Oreochromis niloticus). Nile tilapia fingerlings (initial weight 3.13 ± 0.03 g) were fed diets supplemented with 0, 50, 100, or 150 mg kg⁻ UH for 60 days. The findings demonstrated that dietary supplementation with the hexane fraction of Ulva fasciata extract (UH150, UH100, and UH50) significantly increased final weight gain, specific growth rate, and improved feed conversion ratio compared to UH0 (control diet). According to the intestinal villi histomorphometric evaluation, fish that received UH exhibited improvements in villi length, goblet cell numbers, and intervillous spaces, particularly in UH100 (p < 0.05). However, UH150 demonstrated the most significant improvements in villi width. The highest WBC counts, phagocytic activity, lysozyme activity, superoxide dismutase and catalase activity-alongside normal ranges for hematological and biochemical parameters-were detected in fish that received 100 mgkg UH. The Ulva hexane fraction extract meals at 50, 100, and 150 mg kg triggered upregulation of growth hormone receptor (GHr), insulin-like growth factor (IGF-1), myostatin (MSTN), tumor necrosis factor alpha (TNF-α), heat shock protein 70 (HSP 70), fatty acid synthase (FAS), and lipoprotein lipase (LPL) with the best results being stated in UH150. In conclusion, UH dietary inclusion improved growth performance, feed utilization efficiency, and immune-physiological response of Nile tilapia. - Source: PubMed
Publication date: 2026/05/04
El-Nokrashy Asmaa MHassan Sara SElshafey Ahmed EMohamed Radi A - Genome-wide association studies (GWAS) based on single-step genomic BLUP (ssGBLUP) commonly assume equal single nucleotide polymorphism (SNP) variances, which may not reflect the biological architecture of complex traits. Alternative weighting strategies can increase detection power but may affect stability. This study evaluated how different SNP weighting approaches influence genomic region detection and biological interpretation of ribeye area (REA) and subcutaneous fat thickness (SFT) in Guzerá cattle. Phenotypic records from 2729 animals and genotypes from 1405 individuals (43,039 SNPs after quality control) were analyzed. Heritabilities were estimated using Restricted Maximum Likelihood (REML), and GWAS were conducted under five approaches: unweighted method (UM), quadratic method (QM), and three Non-Linear A strategies with weighting constants (1.125, 1.2, and 1.5). Genomic windows of 20 adjacent SNPs explaining ≥0.5% of the additive genetic variance (AGV) were considered significant. Recurrent regions were prioritized, and functional enrichment analyses (KEGG, GO, and MeSH) were performed. Heritability estimates were moderate for REA (0.26 ± 0.05) and SFT (0.22 ± 0.04). Weighted approaches increased detection sensitivity. For REA, UM identified 10 windows, whereas QM and A_1.5 detected 24 and 31 windows. For SFT, UM identified 8 windows, while QM and A_1.5 detected 30 and 23 windows. Recurrent chromosomes included 2, 4, 6, 12, 16, 19, and 22 for REA, and 2, 3, 5, 7, 11, 17, and 22 for SFT. Key genes included , , and . Enrichment highlighted pathways related to muscle growth and lipid metabolism. SNP-weighted GWAS increased detection sensitivity but involved trade-offs between signal amplification and stability. Integrating weighting strategies improves biological interpretation and supports robust candidate gene identification for genomic selection. - Source: PubMed
Publication date: 2026/03/28
Dos Reis Hugo BorgesMaiorano Amanda MarchiOliveira ElisângelaTonetto FilippiBaldi FernandoFragomeni Breno de OliveiraFerraz José Bento Sterman - Facioscapulohumeral muscular dystrophy (FSHD) is a gain-of-function genetic disorder caused by the loss of repressive epigenetic marks at the D4Z4 macrosatellite repeat array on chromosome 4q35. This epigenetic relaxation, when combined with a permissive 4q distal haplotype, defines the FSHD-permissive allele. Its transcription leads to the aberrant expression in skeletal muscle of the double homeobox transcription factor DUX4 (a gene normally confined to the earliest stages of embryogenesis), disrupting muscle homeostasis and triggering progressive degeneration. Over the past decade, extensive genetic and mechanistic studies have transformed the FSHD landscape. Despite the different genetic causes and the mosaic, temporally sporadic, spatially restricted nature of FSHD, a unified genetic model has emerged. Although the exact role of DUX4 in disease pathogenesis remains to be fully deciphered, a substantial body of evidence implicates it as the central driver of pathology. It is therefore an appealing therapeutic target, and several clinical trials are now underway to determine if suppressing its expression or activity is therapeutic. One of the current challenges in assessing these therapies is the identification of biomarkers capable of capturing disease activity, severity, and target engagement. This is especially challenging with a disease, like FSHD, that progresses slowly and heterogeneously. Progress in identifying biomarkers for potential clinical use marks a turning point for FSHD studies that can pave the way for therapies targeting the root cause of the disease. Here, we integrate what is known about the genetic and epigenetic mechanisms of DUX4 derepression with emerging evidence for spatiotemporal DUX4 toxicity in muscle. We argue that the mosaic expression of DUX4 has direct consequences for the design of biomarkers, the selection of biopsy muscles and sampling sites, and the appropriate endpoints in clinical trials. Finally, we outline a pragmatic approach to align DUX4-targeted and downstream therapies with biomarker strategies that are realistic for FSHD trial design. - Source: PubMed
Publication date: 2026/03/31
Mariot VirginieBloch Robert JBadiani RajBugiardini EnricoDumonceaux Julie