• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

NF κB and Kidney Injury
Conclusion As a critical regulator of inflammation and cell survival, the NFκB pathway is a promising target for diagnosing and treating kidney diseases. For modulation of the NFκB pathway in the clinic, a number of molecules can effectively inhibit NFκB signaling by targeting the receptors, associated adaptors, IKKs, IκBs and transcriptional regulators (144). There is further clinical evidence on small-molecule inhibitors of IKKα and NIK from recent trials on anti-cancer therapies (145). These clinical trials showed that the cancer-selective pharmacodynamic response of DTP3, the co...
Source: Frontiers in Immunology - April 15, 2019 Category: Allergy & Immunology Source Type: research

FOXO1 inhibition potentiates endothelial angiogenic functions in diabetes via suppression of ROCK1/Drp1-mediated mitochondrial fission
Publication date: July 2018Source: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1864, Issue 7Author(s): Yundi Shi, Shengjun Fan, Di Wang, Tianru Huyan, Jinwen Chen, Jiyun Chen, Jing Su, Xin Li, Zhuofei Wang, Shiyu Xie, Caihong Yun, Xuejun Li, Lu TieAbstractDiabetes-induced endothelial cell (EC) dysfunction and neovascularization impairment constitute vascular complications with limited treatment regimens. Transcription factor FOXO1 is a key angiogenic regulator and plays a pathologic role in progression of diabetes. The present study was designed to determine the involvement of FOXO1 in impaired...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - July 10, 2018 Category: Molecular Biology Source Type: research

FOXO1 inhibition potentiates endothelial angiogenic functions in diabetes via suppression of ROCK1/Drp1-mediated mitochondrial fission.
Abstract Diabetes-induced endothelial cell (EC) dysfunction and neovascularization impairment constitute vascular complications with limited treatment regimens. Transcription factor FOXO1 is a key angiogenic regulator and plays a pathologic role in progression of diabetes. The present study was designed to determine the involvement of FOXO1 in impaired EC function and post-ischemic neovascularization in diabetes and investigate underlying mechanisms. We found that FOXO1-selective inhibitor AS1842856 improved blood flow recovery and capillary density in ischemic hindlimb, and rescued the delay of wound closure with...
Source: Biochimica et Biophysica Acta - April 11, 2018 Category: Biochemistry Authors: Shi Y, Fan S, Wang D, Huyan T, Chen J, Chen J, Su J, Li X, Wang Z, Xie S, Yun C, Li X, Tie L Tags: Biochim Biophys Acta Source Type: research

Endothelial deletion of mTORC1 protects against hindlimb ischemia in diabetic mice via activation of autophagy, attenuation of oxidative stress and alleviation of inflammation.
In conclusion, our present study demonstrates that endothelial mTORC1 deletion protects against hindlimb ischemic injury in diabetic mice possibly via activation of autophagy, attenuation of oxidative stress and alleviation of inflammation. Therapeutics targeting mTORC1 may therefore represents a promising strategy to rescue limb ischemia in diabetes mellitus. PMID: 28473248 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - May 1, 2017 Category: Biology Authors: Fan W, Han D, Sun Z, Ma S, Gao L, Chen J, Li X, Li X, Fan M, Li C, Hu D, Wang Y, Cao F Tags: Free Radic Biol Med Source Type: research

Restoration of Hydrogen Sulfide Production in Diabetic Mice Improves Reparative Function of Bone Marrow Cells.
CONCLUSIONS: -Decreased CSE-mediated H2S bioavailability is an underlying source of BMC dysfunction in diabetes. Our data indicate that H2S and overexpression of CSE in diabetic BMCs may rescue their dysfunction and open novel avenues for cell-based therapeutics of CLI in diabetic patients. PMID: 27660293 [PubMed - as supplied by publisher]
Source: Circulation - September 21, 2016 Category: Cardiology Authors: Cheng Z, Garikipati V, Nickoloff E, Wang C, Polhemus DJ, Zhou J, Benedict C, Khan M, Verma SK, Rabinowitz JE, Lefer D, Kishore R Tags: Circulation Source Type: research

Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Promotes Angiogenesis and Ischemia-Induced Neovascularization Via NADPH Oxidase 4 (NOX4) and Nitric Oxide-Dependent Mechanisms Coronary Heart Disease
Conclusions This is the first report demonstrating that TRAIL can promote angiogenesis following hindlimb ischemia in vivo. The angiogenic effect of TRAIL on human microvascular endothelial cell-1 cells is downstream of fibroblast growth factor-2, involving NOX4 and nitric oxide signaling. These data have significant therapeutic implications, such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with cardiovascular disease and diabetes.
Source: JAHA:Journal of the American Heart Association - November 16, 2015 Category: Cardiology Authors: Di Bartolo, B. A., Cartland, S. P., Prado-Lourenco, L., Griffith, T. S., Gentile, C., Ravindran, J., Azahri, N. S. M., Thai, T., Yeung, A. W. S., Thomas, S. R., Kavurma, M. M. Tags: Coronary Heart Disease Source Type: research