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Last update 08 May 2025

GDF5

Last update 08 May 2025

Basic Info

Synonyms

BMP-14, BMP14, Bone morphogenetic protein 14

+ [12]

Introduction

Growth factor involved in bone and cartilage formation. During cartilage development regulates differentiation of chondrogenic tissue through two pathways. Firstly, positively regulates differentiation of chondrogenic tissue through its binding of high affinity with BMPR1B and of less affinity with BMPR1A, leading to induction of SMAD1-SMAD5-SMAD8 complex phosphorylation and then SMAD protein signaling transduction (PubMed:15530414, PubMed:21976273, PubMed:24098149, PubMed:25092592). Secondly, negatively regulates chondrogenic differentiation through its interaction with NOG (PubMed:21976273). Required to prevent excessive muscle loss upon denervation. This function requires SMAD4 and is mediated by phosphorylated SMAD1/5/8 (By similarity). Binds bacterial lipopolysaccharide (LPS) and mediates LPS-induced inflammatory response, including TNF secretion by monocytes (PubMed:11276205).

Drugs associated with GDF5

M-1673

Target

GDF5

Mechanism

GDF5 modulators

Active Org.

Merck KGaA

Originator Org.

Merck KGaA

Active Indication

Osteoarthritis

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MD-05

Target

GDF5

Mechanism

GDF5 modulators

Active Org.-

Originator Org.

BioNet Pharma GmbH

Active Indication-

Inactive Indication

Periodontal Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MD-08

Target

GDF5

Mechanism

GDF5 modulators

Active Org.-

Originator Org.

BioNet Pharma GmbH

Active Indication-

Inactive Indication

Periodontal Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with GDF5

EUCTR2005-003391-37-DE

/ Not yet recruitingNot Applicable

Pilot Study on Safety and explorative Efficacy of MD05 in Comparison with the Medical Device Beta-TCP Mixed with Autogenous Bone Material in Patients Undergoing Two-Stage Unilateral Maxillary Sinus Floor Augmentation - Sinus Lift Study

Start Date05 Dec 2005

Sponsor / Collaborator

BioNet Pharma GmbH

NCT00520377

/ Unknown statusPhase 2

Pilot Study on Safety and Efficacy of MD05 in Comparison With Beta-TCP in Patients Undergoing Sinus Floor Augmentation

The primary objective is the area of newly formed bone (%) as assessed by histomorphometry with either MD05 or beta-TCP.

Start Date01 Jan 2005

Sponsor / Collaborator

BioNet Pharma GmbH

[+1]

100 Clinical Results associated with GDF5

100 Translational Medicine associated with GDF5

0 Patents (Medical) associated with GDF5

880

Literatures (Medical) associated with GDF5

31 Dec 2025·Artificial Cells, Nanomedicine, and Biotechnology

Human tendon stem/progenitor cell-derived extracellular vesicle production promoted by dynamic culture

Article

Author: Ciardulli, Maria Camilla ; Maffulli, Nicola ; Forsyth, Nicholas R. ; Della Porta, Giovanna ; Giordano, Emanuele ; Lamparelli, Erwin Pavel ; Lovecchio, Joseph ; Dale, Tina P. ; Clerici, Marta

Tendon injuries significantly impact quality of life, prompting the exploration of innovative solutions beyond conventional surgery. Extracellular Vesicles (EVs) have emerged as a promising strategy to enhance tendon regeneration. In this study, human Tendon Stem/Progenitor Cells (TSPCs) were isolated from surgical biopsies and cultured in a Growth-Differentiation Factor-5-supplemented medium to promote tenogenic differentiation under static and dynamic conditions using a custom-made perfusion bioreactor. Once at 80% confluence, cells were transitioned to a serum-free medium for conditioned media collection. Ultracentrifugation revealed the presence of vesicles with a 10⁶ particles/mL concentration and sub-200nm diameter size. Dynamic culture yielded a 3-fold increase in EV protein content compared to static culture, as confirmed by Western-blot analysis. Differences in surface marker expression were also shown by flow cytometric analysis. Data suggest that we efficiently developed a protocol for extracting EVs from human TSPCs, particularly under dynamic conditions. This approach enhances EV protein content, offering potential therapeutic benefits for tendon regeneration. However, further research is needed to fully understand the role of EVs in tendon regeneration.

01 Jul 2025·Cellular Signalling

LncRNA AC100865.1 regulates macrophage adhesion and ox-LDL intake through miR-7/GDF5 pathway

Article

Author: Chen, Jinfeng ; Chen, Baofeng ; Liu, Xiangying ; Liu, Xiangyang ; Liang, Jiarong ; Chen, Yunxian ; Ren, Yong

OBJECTIVESCardiovascular disease (CVD) accounts for over 40 % of deaths related to diseases among residents. Atherosclerosis (AS) and its associated thrombosis are the primary causes of CVD. LncRNA AC100865.1, a newly identified lncRNA, has shown potential as a diagnostic biomarker for AS. This study aims to evaluate the therapeutic value of lncRNA AC100865.1 in AS.METHODSReal-time PCR was conducted to assess the relative expression of lncRNA AC100865.1 in Peripheral Blood Mononuclear Cell (PBMC) samples from 50 CVD patients and 50 healthy controls. lncRNA AC100865.1 was overexpressed in RAW264.7 cells to measure its effects on adhesion and oxidized low-density lipoprotein (ox-LDL) uptake. Flow cytometry was utilized to identify the pathway mediating these processes. The luciferase assay and knockout rescue experiments were performed to elucidate the downstream signaling pathways involved.RESULTSlncRNA AC100865.1 expression was found to be downregulated in CVD patients. Overexpression of lncRNA AC100865.1 significantly enhanced the adhesion capacity of RAW264.7 cells. Luciferase reporter assays and flow cytometry indicated that this effect is mediated through the miR-7/GDF5/p38/LFA-1 pathway. Furthermore, lncRNA AC100865.1 notably increased ox-LDL uptake by macrophages via upregulation of CD36 expression.CONCLUSIONOverexpression of lncRNA AC100865.1 enhances the adhesion of RAW264.7 cells through the miR-7/GDF5/p38/LFA-1 pathway and increases ox-LDL uptake by elevating CD36 levels. These findings suggest that circulating lncRNA AC100865.1 may serve not only as an early diagnostic marker for CVD but also as a potential therapeutic target, offering new prospects for CVD treatment.

01 Jun 2025·Experimental Eye Research

Involvement of TGF-β signaling pathway-associated genes in the corneal endothelium of patients with Fuchs endothelial corneal dystrophy

Article

Author: Vaitinadapoule, Hanielle ; Tourtas, Theofilos ; Koizumi, Noriko ; Thuret, Gilles ; Schlötzer-Schrehardt, Ursula ; Travers, Gauthier ; Honda, Tetsuro ; Aouimeur, Ines ; Gain, Philippe ; He, Zhiguo ; Kruse, Friedrich ; Okumura, Naoki ; Yuasa, Taichi ; Inagaki, Soichiro ; Nakagawa, Tatsuya

This study investigated the involvement of TGF-β signaling pathway-associated genes in the pathogenesis of Fuchs endothelial corneal dystrophy (FECD). The RNA-sequencing analysis of corneal endothelial cells (CECs) from FECD patients revealed significant alterations in multiple TGF-β superfamily genes, with 9 genes upregulated (including BMP6, GDF5, and TGF-β2) and 10 genes downregulated (including BMP2, NOG, and INHBA) compared to controls. Quantitative PCR validation confirmed the elevated expression of GDF5 (3.35-fold in non-expanded and 7.66-fold in expanded TCF4), TGF-β2 (6.17-fold and 11.5-fold), and TGF-β1 (1.78-fold and 1.58-fold) in FECD patients with and without TCF4 trinucleotide repeat expansion. Ex-vivo experiments using donor corneas demonstrated that TGF-β2 stimulation significantly increased the expression of extracellular matrix (ECM) components associated with guttae formation, including fibronectin, types I and VI collagens, and other matrix proteins. Immunofluorescence confirmed increased fibronectin protein expression in the corneal endothelium following TGF-β1 or TGF-β2 treatment. This study provides the first comprehensive analysis of TGF-β superfamily involvement in FECD and suggests that GDF5, found to be upregulated in FECD, may contribute to the disease process. These findings further indicate that dysregulation of TGF-β signaling pathways drives the characteristic ECM accumulation in FECD, potentially offering new therapeutic targets for this progressive corneal disease involving fibrosis-related alterations. Future research is warranted to clarify GDF5's specific role and mechanistic impact on FECD pathogenesis.

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