Serum MCP-1 and TGF-β1 levels were both higher in PM/DM patients complicated with ILD compared with patients with pulmonary infections and normal controls.
A statistically significant change in the transcription activity of TGFβ1 in patients with and without diabetes (P = 0.018) and patients with and without metabolic syndrome (P = 0.023) was shown that on the 84th day of therapy.
MMP‑2 expression was decreased, and the expressions of WISP‑1, TIMP‑2, collagens, and canonical Wnt and TGF‑β1/Smad3 pathway‑related proteins were increased in the myocardia of the diabetes model rats.
More importantly, clinical research revealed that gradually decreased DNA methylation in the TGFβ1 regulatory region was also present in patients with diabetes and DN.
These changes also correlated with increased TGFβ1 activity, gene expression in the left kidney and elevated active TGFβ1 in the plasma of T1DM rats compared to control.
Our results demonstrate that curcumin suppresses diabetes-associated collagen synthesis in rat myocardium not only by inhibiting TGF-β1 production and canonical Smad signaling but also by blocking the non-canonical AMPK/p38 MAPK pathway.
In this study, pathological changes, expression of COL4 a1-a5 chains (<i>Col4a1-a5</i>), COL4 distribution and protein and TGFB1 and SMAD3 protein were first assessed in a rat model of diabetes.
Total glomeruli number in D and DH, were increased by ASE that also reduced renal fibrosis in both groups by decreasing collagen IV and TGF-β1 expression.
Similar to that of collagen, the expression of transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor (VEGF), and insulin-like growth factor 1 receptor (IGF-1R) significantly decreased in DM compared with that in C. Higher recovery of TGF-β1 and VEGF was detected in groups with earlier treatment, whereas the IGF-1R level was identically elevated in all treated groups.
Thus we propose that Cx43 might enhance the activation of Nrf2/ARE pathway by means of inhibiting c-Src activity to hinder the nuclear export of Nrf2, and then reduce expression of FN, ICAM-1 and TGF-β1, ultimately attenuating renal fibrosis in diabetes.
Renal damage following Alloxan-induced diabetes is associated with generation of reactive oxygen species, alterations of p53, TGF-β1, and extracellular matrix metalloproteinases in rats.
In a streptozotocin-induced diabetes mouse model, Nrf2(-/-) mice have delayed wound closure rates compared with Nrf2(+/+) mice, which is, at least partially, due to greater oxidative DNA damage, low transforming growth factor-β1 (TGF-β1) and high matrix metalloproteinase 9 (MMP9) expression, and increased apoptosis.
A novel association between TGFb1 and ADAMTS4 in coronary artery disease: A new potential mechanism in the progression of atherosclerosis and diabetes.
Indeed, DHT counteracted the effect of diabetes on the mechanical nociceptive threshold, pre- and post-synaptic components, glutamate release, astrocyte immunoreactivity, and expression of interleukin-1β (IL1β), while 3α-diol was effective on tactile allodynia threshold, glutamate release, astrocyte immunoreactivity and the expression of substance P, toll-like receptor 4, tumor necrosis factor-α, transforming growth factor β-1, IL1β, and translocator protein.
Among three TGFβ isoforms, TGF-β1 and β3 were upregulated in response to wounding in NL corneal epithelial cells (CECs), whereas the latter was greatly suppressed by hyperglycemia in rat type 1 and 2 and mouse type 1 DM models.
Since TGF-beta1 is well known to stimulate the PAI-1 promoter, we suggest that TGF-beta1 and PAI-1 together constitute a positive feedback loop in the development of renal fibrosis in diabetes.
Here we determined whether there is an association between serum levels of TGF-beta1 and the risk factors for progression of clinically relevant renal disorders in 186 black and 147 white adults, none of whom had kidney disease or diabetes.
These findings comprise physiological mechanisms that could be important in diseases where TGF-beta1 plasma level is increased as in gestational diabetic mothers or patients with diabetes mellitus.