Xiao-Ru Huang

Expression of macrophage migration inhibitory factor in acute ischemic myocardial injury.

Angiotensin II induces connective tissue growth factor and collagen I expression via transforming growth factor-beta-dependent and -independent Smad pathways: the role of Smad3.

Disruption of Smad4 impairs TGF-β/Smad3 and Smad7 transcriptional regulation during renal inflammation and fibrosis in vivo and in vitro.

Diverse roles of TGF-β receptor II in renal fibrosis and inflammation in vivo and in vitro.

Asiatic acid inhibits liver fibrosis by blocking TGF-beta/Smad signaling in vivo and in vitro.

Smad7 inhibits angiotensin II-induced hypertensive cardiac remodelling.

Deficiency of Smad7 enhances cardiac remodeling induced by angiotensin II infusion in a mouse model of hypertension.

C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration.

miR-29b as a therapeutic agent for angiotensin II-induced cardiac fibrosis by targeting TGF-β/Smad3 signaling.

Chaihuang-Yishen granule inhibits diabetic kidney disease in rats through blocking TGF-β/Smad3 signaling.

Latent transforming growth factor-β1 protects against bleomycin-induced lung injury in mice.

Opposing roles for Smad2 and Smad3 in peritoneal fibrosis in vivo and in vitro.

Partial loss of Smad7 function impairs bone remodeling, osteogenesis and enhances osteoclastogenesis in mice.

MicroRNA-29b inhibits peritoneal fibrosis in a mouse model of peritoneal dialysis.

microRNA-29b prevents liver fibrosis by attenuating hepatic stellate cell activation and inducing apoptosis through targeting PI3K/AKT pathway.

Renoprotective effect of berberine on type 2 diabetic nephropathy in rats.

Smad7 protects against chronic aristolochic acid nephropathy in mice.

Deletion of Smad3 improves cardiac allograft rejection in mice.

Treatment of renal fibrosis by rebalancing TGF-β/Smad signaling with the combination of asiatic acid and naringenin.

N-Acetyl-seryl-aspartyl-lysyl-proline Alleviates Renal Fibrosis Induced by Unilateral Ureteric Obstruction in BALB/C Mice.

TGF-β/Smad3 signalling regulates the transition of bone marrow-derived macrophages into myofibroblasts during tissue fibrosis.

Peritoneal inflammation and fibrosis in C-reactive protein transgenic mice undergoing peritoneal dialysis solution treatment.

C-Reactive Protein Promotes Diabetic Kidney Disease in db/db Mice via the CD32b-Smad3-mTOR signaling Pathway.

Validity of leptin receptor-deficiency (db/db) type 2 diabetes mellitus mice as a model of secondary osteoporosis.

Inflammatory macrophages can transdifferentiate into myofibroblasts during renal fibrosis.

The pattern recognition receptor, Mincle, is essential for maintaining the M1 macrophage phenotype in acute renal inflammation.

N-acetyl-seryl-aspartyl-lysyl-proline Mediates the Anti-fibrotic Properties of Captopril in Unilateral Ureteric Obstructed BALB/C Mice.

Macrophage-to-Myofibroblast Transition Contributes to Interstitial Fibrosis in Chronic Renal Allograft Injury.

Smad3 promotes cancer progression by inhibiting E4BP4-mediated NK cell development.

The Regulatory T-cell Transcription Factor Foxp3 Protects against Crescentic Glomerulonephritis.

Defective CFTR leads to aberrant β-catenin activation and kidney fibrosis.

The proto-oncogene tyrosine protein kinase Src is essential for macrophage-myofibroblast transition during renal scarring.

TGF-β Mediates Renal Fibrosis via the Smad3-Erbb4-IR Long Noncoding RNA Axis.

Lethal (3) malignant brain tumor like 2 (L3MBTL2) protein protects against kidney injury by inhibiting the DNA damage-p53-apoptosis pathway in renal tubular cells.