Last update 19 Sep 2024

FSTL3

Last update 19 Sep 2024

Basic Info

Synonyms

FLRG, follistatin like 3, Follistatin-like protein 3

+ [4]

Introduction

Isoform 1 or the secreted form is a binding and antagonizing protein for members of the TGF-beta family, such us activin, BMP2 and MSTN. Inhibits activin A-, activin B-, BMP2- and MSDT-induced cellular signaling; more effective on activin A than on activin B. Involved in bone formation; inhibits osteoclast differentiationc. Involved in hematopoiesis; involved in differentiation of hemopoietic progenitor cells, increases hematopoietic cell adhesion to fibronectin and seems to contribute to the adhesion of hematopoietic precursor cells to the bone marrow stroma. Isoform 2 or the nuclear form is probably involved in transcriptional regulation via interaction with MLLT10.

Drugs associated with FSTL3

ELV-101

Target

FSTL3

Mechanism

FSTL3 inhibitors

Active Org.

Elevian, Inc.Startup

Originator Org.

Elevian, Inc.Startup

Active Indication

Cardiovascular Diseases [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with FSTL3

100 Translational Medicine associated with FSTL3

0 Patents (Medical) associated with FSTL3

293

Literatures (Medical) associated with FSTL3

02 Sep 2024·Journal of Bone and Mineral Research

The comparative effect of teriparatide and denosumab on activins, follistatins, and inhibins in women with postmenopausal osteoporosis

Article

Author: Anastasilakis, Athanasios D ; Savvidis, Matthaios ; Mantzoros, Christos S ; Polyzos, Stergios A ; Makras, Polyzois

AbstractThe activins–follistatins–inhibins (AFI) hormonal system affects bone metabolism. Treatments that alter bone metabolism may also alter the AFI molecules. In this non-randomized, open-label, head-to-head comparative study, circulating levels of the AFI system were evaluated in postmenopausal women with osteoporosis treated for 12 mo with either teriparatide (n = 23) or denosumab (n = 22). Τeriparatide treatment increased activin B (P=.01) and activin AB (P=.004) and the ratios activin A/follistatin (P=.006), activin B/follistatin (P=.007), activin AB/follistatin (P<.001), and activin AB/ follistatin-like 3 (FSTL3) (P=.034). The significant P for trend in group × time interactions of activins B and AB and of the ratio activin AB/FSTL3 remained robust after adjustment for BMI and LS BMD but it was lost for activin B after adjustment for previous antiresorptive treatment. The effect of teriparatide on BMD was attenuated when it was adjusted for baseline activins levels or their 12-mo changes. No changes were observed after denosumab treatment. In conclusion, activins B and AB, as well as the ratios of all activins to follistatin and of activin AB to FSTL3 increased with teriparatide treatment, possibly in a compensatory manner. Future studies are needed to study the potentially important role activins may play in bone biology and any associations with the effect of teriparatide on BMD.Clinical Trials identifier: NCT04206618. ClinicalTrials.gov https://clinicaltrials.gov/search?term=NCT04206618.

01 Jul 2024·Brain, Behavior, and Immunity

Plasma proteomic biomarkers and the association between poor cardiovascular health and incident dementia: The UK Biobank study

Article

Author: Beydoun, Hind A ; Launer, Lenore J ; Meirelles, Osorio ; Evans, Michele K ; Hu, Yi-Han ; Song, Minkyo ; Georgescu, Michael F ; Noren Hooten, Nicole ; Beydoun, May A ; Zonderman, Alan B ; Maino Vieytes, Christian A ; Fanelli-Kuczmarski, Marie T

BACKGROUNDThe study examined how plasma proteome indicators may explain the link between poor cardiovascular health (CVH) and dementia risk.METHODSThe present study involved 28,974 UK Biobank participants aged 50-74y at baseline (2006-2010) who were followed-up for ≤ 15 y for incidence of dementia. CVH was calculated using Life's Essential 8 (LE8) total scores. The scores were standardized and reverse coded to reflect poor CVH (LE8z_rev). OLINK proteomics was available on this sample (k = 1,463 plasma proteins). The study primarily tested the mediating effects of the plasma proteome in LE8z_rev-dementia effect. The total effect was decomposed into "mediation only" or pure indirect effect (PIE), "interaction only" or interaction referent (INTREF), "neither mediation nor interaction" or controlled direct effect (CDE), and "both mediation and interaction" or mediated interaction (INTMED).RESULTSThe study found poorer CVH assessed by LE8z_rev increased the risk of all-cause dementia by 11 % [per 1 SD, hazard ratio, (HR) = 1.11, 95 % CI: 1.03-1.20, p = 0.005). The study identified 11 plasma proteins with strong mediating effects, with GDF15 having the strongest association with dementia risk (per 1 SD, HR = 1.24, 95 % CI: 1.16, 1.33, P < 0.001 when LE8z_rev is set at its mean value) and the largest proportion mediated combining PIE and INTMED (62.6 %; 48 % of TE is PIE), followed by adrenomedullin or ADM. A first principal component with 10 top mediators (TNFRSF1A, GDF15, FSTL3, COL6A3, PLAUR, ADM, GFRAL, ACVRL1, TNFRSF6B, TGFA) mediated 53.6 % of the LE8z_rev-dementia effect. Using all the significant PIE (k = 526) proteins, we used OLINK Insight pathway analysis to identify key pathways, which revealed the involvement of the immune system, signal transduction, metabolism, disease, protein metabolism, hemostasis, membrane trafficking, extracellular matrix organization, developmental biology, and gene expression among others. STRING analysis revealed that five top consistent proteomic mediators were represented in two larger clusters reflecting numerous interconnected biological gene ontology pathways, most notably cytokine-mediated signaling pathway for GDF15 cluster (GO:0019221) and regulation of peptidyl-tyrosine phosphorylation for the ADM cluster (GO:0050730).CONCLUSIONDementia is linked to poor CVH mediated by GDF15 and ADM among several key proteomic markers which collectively explained ∼ 54 % of the total effect.

18 Jun 2024·Journal of the American Heart Association

Prognostic Significance of Proteomics‐Discovered Circulating Inflammatory Biomarkers in Patients With Pulmonary Arterial Hypertension

Article

Author: Bonnet, Sébastien ; Martineau, Sandra ; Provencher, Steeve ; Krishna, Vinod ; Kalyana-Sundaram, Shanker ; Jeyaseelan, Jey ; Boucherat, Olivier ; Potus, François ; Lemay, Sarah-Eve ; Breuils-Bonnet, Sandra ; Yokokawa, Tetsuro

BackgroundPulmonary arterial hypertension (PAH) ultimately leads to right ventricular failure and premature death. The identification of circulating biomarkers with prognostic utility is considered a priority. As chronic inflammation is recognized as key pathogenic driver, we sought to identify inflammation‐related circulating proteins that add incremental value to current risk stratification models for long‐term survival in patients with PAH.Methods and ResultsPlasma levels of 384 inflammatory proteins were measured with the proximity extension assay technology in patients with PAH (n=60) and controls with normal hemodynamics (n=28). Among these, 51 analytes were significantly overexpressed in the plasma of patients with PAH compared with controls. Cox proportional hazard analyses and C‐statistics were performed to assess the prognostic value and the incremental prognostic value of differentially expressed proteins. A panel of 6 proteins (CRIM1 [cysteine rich transmembrane bone morphogenetic protein regulator 1], HGF [hepatocyte growth factor], FSTL3 [follistatin‐like 3], PLAUR [plasminogen activator, urokinase receptor], CLSTN2 [calsyntenin 2], SPON1 [spondin 1]) were independently associated with death/lung transplantation at the time of PAH diagnosis after adjustment for the 2015 European Society of Cardiology/European Respiratory Society guidelines, the REVEAL (Registry to Evaluate Early and Long‐Term PAH Disease Management) 2.0 risk scores, and the refined 4‐strata risk assessment. CRIM1, PLAUR, FSTL3, and SPON1 showed incremental prognostic value on top of the predictive models. As determined by Western blot, FSTL3 and SPON1 were significantly upregulated in the right ventricle of patients with PAH and animal models (monocrotaline‐injected and pulmonary artery banding‐subjected rats).ConclusionsIn addition to revealing new actors likely involved in cardiopulmonary remodeling in PAH, our screening identified promising circulating biomarkers to improve risk prediction in PAH, which should be externally confirmed.

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FSTL3

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