Ask about this productRelated genes to: FSTL1 antibody
- Gene:
- FSTL1 NIH gene
- Name:
- follistatin like 1
- Previous symbol:
- -
- Synonyms:
- FRP, FSL1, OCC1, OCC-1, tsc36
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-06-09
Related products to: FSTL1 antibody
Related articles to: FSTL1 antibody
- Exercise-induced secreted factors (exerkines) are proposed to coordinate systemic health benefits, yet their human tissue sources and the physiological rules governing transcript-to-serum coupling remain incompletely defined. We integrated multi-tissue transcriptomics with matched serial serum profiling to identify exercise-regulated exerkines and determine whether tissue mass moderates their systemic appearance. Sixteen healthy, sedentary young men performed a single treadmill bout calibrated to expend 300 kcal at 70-75% of maximum heart rate. RNA sequencing was performed on periumbilical subcutaneous adipose tissue, vastus lateralis skeletal muscle and whole blood collected before and immediately after exercise, with serial serum quantification up to 120 min post-exercise. Acute exercise altered adipose and muscle transcriptomes, with a minimal whole-blood response, and upregulated LGALS1 (galectin-1), FSTL1 (follistatin-like 1), OGN (osteoglycin) and C1QTNF3 (C1q and tumour necrosis factor-related protein 3) in both tissues. Serum follistatin-like 1 and galectin-1 concentrations increased significantly immediately after exercise and during recovery. Despite robust transcript induction, OGN and C1QTNF3 did not translate into early circulating increases, indicating candidate-specific kinetics and constraints beyond transcript abundance. Moderation models revealed divergent transcript-to-serum coupling: follistatin-like 1 coupling was moderated by tissue mass in both muscle and adipose depots, whereas galectin-1 followed a muscle-dominant additive profile independent of mass scaling. These findings propose galectin-1 and follistatin-like 1 as human exerkines and indicate that body composition regulates systemic exerkine signatures after exercise, providing a mechanistic framework for understanding physiological variability in exercise-induced adaptations. KEY POINTS: Exercise releases circulating factors that may contribute to health benefits, but the human tissues responsible for their production remain unclear. RNA sequencing was performed in human skeletal muscle, subcutaneous adipose tissue and whole blood, with targeted serum protein quantification over 2 h after a single treadmill bout. Exercise increased LGALS1 and FSTL1 transcripts in skeletal muscle and adipose tissue, with concurrent increases in their circulating protein products immediately post-exercise and during recovery, whereas OGN and C1QTNF3 transcripts increased robustly without an early post-exercise elevation in their circulating protein products. Body composition moderated transcript-to-serum coupling: FSTL1 (follistatin-like 1) showed mass-sensitive coupling, whereas LGALS1 (galectin-1) displayed a muscle-dominant additive profile. Galectin-1 and follistatin-like 1 emerge as exercise-induced exerkines whose circulating responses vary with body composition, supporting their prioritization as candidate mediators of exercise-related health benefits and a framework for interpreting physiological heterogeneity in adaptation. - Source: PubMed
Publication date: 2026/05/15
Song JaeseungCho Eun-SukKwon Yu RimPark Jong SukNam Ji SunKim YuSik - Nephrolithiasis is a clinical entity with long-term course, facing rising global prevalence and recurrence rates. Long noncoding RNAs (LncRNAs) have emerged as regulators implicated in the progression of nephrolithiasis, yet the functional role of lncRNA MIR205HG remains poorly characterized. Our research attempted to investigate the function of the lncRNA MIR205HG in calcium oxalate nephrolithiasis and focus on its in-depth competitive endogenous RNA (ceRNA) regulatory network. MIR205HG expression in the Randall's plaque tissues of calcium oxalate (CaOx) nephrolithiasis patients and calcium oxalate monohydrate (COM)-stimulated HK2 cells was examined with GSE117518 dataset from GEO database and RT-qPCR. CCK-8 and flow cytometry assays separately estimated cell viability and apoptosis. DCFH-DA probe and western blotting measured oxidative stress mediators. RT-qPCR also tested miR-5581-3p and follistatin-like protein 1 (FSTL1) expressions. A targeting relationship among MIR205HG, miR-5581-3p and FSTL1 was determined using bioinformatics software and luciferase reporter assays. Besides, cellular morphology was observed and cell adhesion was detected. Western blotting assessed epithelial-mesenchymal transition (EMT) markers. A total of 62 upregulated and 17 downregulated genes were identified. MIR205HG expression was elevated both in the Randall's plaque tissues of calcium oxalate (CaOx) nephrolithiasis patients and COM-stimulated HK2 cells. MIR205HG silencing promoted the viability, inhibited the apoptosis, and ameliorated the oxidative stress in COM-induced HK2 cells. MIR205HG could sequester miR-5581-3p which directly targeted FSTL1. In addition to the impacts on FSTL1 expression, cell viability, apoptosis and oxidative stress, miR-5581-3p inhibitor could also restore the suppressive role of MIR205HG knockdown in the morphological changes, EMT and adhesion of COM-induced HK2 cells. Conclusively, lncRNA MIR205HG participated in the process of CaOx nephrolithiasis through mediating the miR-5581-3p/FSTL1 pathway. - Source: PubMed
Publication date: 2026/05/14
Zhou MinChen ChuntaoZou ZhenhaiFeng FeiDong LiHou ChuantaoWang MingxingZhao LiangdongCao Daojun - The pathogenesis and diagnosis of breast cancer remain the subject of intensive research, as many aspects of these processes still require further elucidation. The dominant component of breast tissue stroma, adipose tissue, is composed of adipocytes, which secrete various cytokines, including adipokines, whose role in breast cancer is not fully understood. - Source: PubMed
Publication date: 2026/03/31
Morawiec Maria-LauraWendlocha DominikaKabut JacekMielczarek-Palacz Aleksandra - The ovary is a central female reproductive organ responsible for producing oocytes and secreting steroid hormones. To investigate the molecular similarities and potential evolutionary origins of the ovary across vertebrates, we integrated publicly available single-cell and single-nucleus transcriptomic data from nine species, including oviparous animals (fish and chicken) and viviparous mammals (mouse, rat, sheep, goat, yak, monkey, and human). - Source: PubMed
Publication date: 2026/04/14
Xue BailingLiu YajingZhou ChenDossybayev KairatBaatar NarantuyaYudin NikolayZhang LinweiYang JiLi MenghuaXu Songsong - The SPARC (secreted protein acidic and rich in cysteine) family represents a unique class of matricellular proteins - including SPARC, SPARCL1, SPOCK1-3, SMOC1-2, and FSTL1 - that regulate extracellular matrix (ECM) dynamics, cell signaling, and tissue homoeostasis. In cancer, their expression is frequently dysregulated, through epigenetic mechanisms, microRNAs, and interactions within the tumor microenvironment (TME). Dysregulation of SPARC family members is most pronounced in aggressive malignancies with SPARC, SPARCL1, SPOCK1, and SPOCK2 most consistently altered. These proteins drive tumor progression through ECM remodeling, epithelial-mesenchymal transition (EMT), maintenance of cancer stemness, immune modulation, and drug resistance acquisition. Their functions are highly context-dependent, exerting either tumor-suppressive or oncogenic effects depending on tissue types and disease stage. While their secreted nature positions family members as promising serum or plasma biomarkers, challenges such as ECM protein undruggability, functional heterogeneity, and the absence of upstream regulators have so far precluded direct therapeutic targeting, with no agents advancing to clinical trials. Nonetheless, indirect strategies leveraging their biology show preclinical promise. This review synthesizes current knowledge on SPARC family structure, regulation, and context-specific functions in cancer-TME interactions, emphasizing their dual roles as modulators of progression and resistance. By integrating mechanistic insights with translational advances, we highlight the emerging utility of SPARC family proteins in precision oncology and underscore the need for deeper understanding to enable effective biomarker development and targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/04/14
Hoe Rachel Huey XuanRamasamy Thamil SelveeSinniah AjanthaAyob Ain Zubaidah