Smad proteins x TGF-β1

Last update 08 May 2025

Basic Info

Related Targets

Smad proteinsTGF-β1

Drugs associated with Smad proteins x TGF-β1

dNP-15

Target

Smad proteins x TGF-β1

Mechanism

Smad proteins inhibitors [+1]

Active Org.

Third Military Medical University [+1]

Originator Org.

Chengdu Huitai Biomedical Co., Ltd.

Active Indication

Idiopathic Pulmonary Fibrosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Smad proteins x TGF-β1

100 Translational Medicine associated with Smad proteins x TGF-β1

0 Patents (Medical) associated with Smad proteins x TGF-β1

4,523

Literatures (Medical) associated with Smad proteins x TGF-β1

31 Dec 2025·Renal Failure

Carthamin yellow-loaded glycyrrhetinic acid liposomes alleviate interstitial fibrosis in diabetic nephropathy

Article

Author: Jin, Juan ; Ren, Peiyao ; He, Wenfang ; Zheng, Danna ; Zhao, Li ; Wang, Yifei

OBJECTIVESTo investigate the therapeutic efficacy of Carthamin yellow (CY)-loaded glycyrrhetinic acid (GA) liposomes in treating diabetic nephropathy (DN), particularly in alleviating renal interstitial fibrosis and improving kidney function.METHODSCY-loaded GA liposomes were prepared and characterized for structural stability and controlled release. DN rat models were treated with CY-loaded GA liposomes, and kidney pathology, function, collagen deposition, and TGF-β1 expression were evaluated. The effects of CY-loaded GA liposomes were compared to Vitamin E and CY alone. In vitro experiments with TGF-β1-stimulated human renal interstitial fibroblasts (hRIFs) examined the effects of CY-loaded GA liposomes on cell proliferation and the expression of fibrotic markers. Mechanistic studies assessed the role of the TGFBR1/Smad2/Smad3 pathway using TGFBR1 overexpression experiments.RESULTSThe CY-loaded GA liposomes exhibited a stable structure and controlled release profile. In DN rats, treatment with CY-loaded GA liposomes significantly alleviated kidney damage, improved kidney function, reduced collagen deposition and fibrosis, and downregulated TGF-β1 expression, showing superior effects compared to Vitamin E or CY alone. In TGF-β1-stimulated hRIFs, CY-loaded GA liposomes effectively suppressed cell proliferation and reduced the expression of Cyclin D1, PCNA, fibronectin, and collagen I. The inhibitory effects were stronger than CY alone and were mediated by the inactivation of the TGFBR1/Smad2/Smad3 pathway, as confirmed by TGFBR1 overexpression studies.CONCLUSIONSCY-loaded GA liposomes demonstrated significant therapeutic efficacy in alleviating renal interstitial fibrosis in DN by targeting the TGFBR1/Smad2/Smad3 pathway. This novel drug delivery system provides a promising approach for the treatment of DN.

01 Jun 2025·Phytomedicine

Diabetic wound healing breakthrough: theaflavin-3, 3’-digallate nanoparticles@hydrogel activates the TGF-β1/SMAD3 pathway

Article

Author: Miao, Jianyin ; Zhai, Qingqing ; Wu, Ling ; Jia, Diyi ; Xu, Yan ; Kong, Ziyu ; Dong, Xu ; Zhang, Dan ; Liu, Zenghui

BACKGROUNDDiabetes patients face an elevated wound infection susceptibility and delayed healing processes. Currently, no existing literature has reported on the effect and mechanism of theaflavin-3, 3'-digallate nanoparticles (TFDG NPS) and TFDG NPS@hydrogels on diabetic wounds.PURPOSEGiven that the treatment options for diabetic wound are limited, the aim of this study is to develop an innovative therapeutic approach to address diabetic wounds.METHODSThe TFDG NPS were prepared using ionic cross-linking, and they were then characterized. The biocompatibility of the TFDG NPS and TFDG NPS@hydrogel was assessed using a Cell Counting Kit-8 (CCK-8) assay and live/dead staining on HK-2 cells in vitro. Diabetic ICR mice were induced through intraperitoneal injection of streptozocin (STZ). They were then subjected to the creation of two full-thickness wounds on their dorsal areas. The effect and mechanism of the TFDG NPS and TFDG NPS@hydrogel on wound healing in diabetic mice were evaluated using a histological analysis, a western blot analysis, and molecular docking.RESULTSThe optimal TFDG NPS proportion was found to be TFDG:Gelatin (Gel):Chitosan (CS) = 2:1:1. Images photographed using a transmission electron microscope (TEM) revealed that the TFDG NPS appeared spherical, with a diameter of approximately 140 ± 20 nm. The favorable bio-compatibility of the TFDG NPS and TFDG NPS@hydrogel was confirmed using cell experiments. Animal studies demonstrated that both the TFDG NPS and TFDG NPS@hydrogel enhanced collagen fiber accumulation and new blood vessel density, reduced F4/80 infiltration, and upregulated the expression levels of TGF-β1, SMAD3, Collagen I, and α-SMA. The potential mechanism may involve activation of the TGF-β1/SMAD3 pathway, stimulating the secretion of Collagen I and α-SMA, and thereby facilitating wound closure in diabetic mice. The molecular docking results confirmed a high affinity between TFDG and TGF-β1/SMAD3.CONCLUSIONTFDG NPS and TFDG NPS@hydrogel promoted wound closure in diabetic mice through the TFG-β1/SMAD3 pathway, thus exhibiting promising therapeutic potential for diabetic wound treatment.

01 Jun 2025·Toxicology and Applied Pharmacology

Breaking the scar barrier: The anti-fibrotic and hemodynamic benefits of total salvianolic acid in hypertrophic scars

Article

Author: Wu, Xinying ; Shi, Jun ; Luo, Xi ; Zhang, Qiaoju ; Zheng, Yuwen ; Zheng, Junqiao

Hypertrophic scars (HS) affect up to 70 % of individuals following deep dermal injuries, burns, or surgical procedures, leading to significant functional impairments and psychological distress. Despite their high prevalence, effective therapeutic options remain limited, and the underlying pathophysiology is not fully elucidated. This study integrates network pharmacology, molecular docking, and in vivo experimentation to investigate the therapeutic potential of total salvianolic acid (TSA) from Salvia miltiorrhiza in HS treatment. A systematic pharmacology approach identified 186 target proteins, highlighting TGF-β1, Smad3, IL-2, and IL-4 as key modulators of fibrosis and inflammation. Molecular docking confirmed high-affinity interactions between TSA's active components and these targets. TSA significantly reduced scar elevation, fibrosis, and collagen deposition in a rabbit ear hypertrophic scar model, restoring tissue architecture and improving hemorheological parameters. Histological and immunohistochemical analyses confirmed TSA's ability to suppress TGF-β/Smad signaling, downregulate inflammatory cytokines and normalize collagen dynamics. These findings provide compelling evidence that TSA is a multi-targeted, pharmacologically active compound with promising anti-fibrotic and microcirculatory benefits, paving the way for novel therapeutic strategies in HS management. This study establishes a scientific foundation for TSA-based interventions, with potential clinical implications in regenerative medicine and scar therapy.

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