ArticleJournal of cellular and molecular medicine2014
Inhibition of MAPK-mediated ACE expression by compound C66 prevents STZ-induced diabetic nephropathy.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Exploring the renoprotective potential of Beta vulgaris in diabetic nephropathy: an integrated network pharmacology, molecular docking and dynamics simulation study.Molecular diversity · 2026Article
- Curcumin and Gut Microbiota: A Narrative Overview with Focus on Glycemic Control.International journal of molecular sciences · 2024Review
- Therapeutic Effects of Curcumin Derivatives against Obesity and Associated Metabolic Complications: A Review of In Vitro and In Vivo Studies.International journal of molecular sciences · 2023Review
- Overview of Curcumin and Piperine Effects on Glucose Metabolism: The Case of an Insulinoma Patient's Loss of Consciousness.International journal of molecular sciences · 2023Review
- Curcumin analog C66 alleviates inflammatory colitis by inhibiting the activation of NF-κB.Inflammopharmacology · 2022Article
- Efficacy of the monocarbonyl curcumin analog C66 in the reduction of diabetes-associated cardiovascular and kidney complications.Molecular medicine (Cambridge, Mass.) · 2022Review
- The Role of PKC-MAPK Signalling Pathways in the Development of Hyperglycemia-Induced Cardiovascular Complications.International journal of molecular sciences · 2022Review
- Protective Role of Nrf2 in Renal Disease.Antioxidants (Basel, Switzerland) · 2020Review
- A Synthetic Curcuminoid Analog, (2Molecules (Basel, Switzerland) · 2020Article
- Kruppel-like factor 4 improves obesity-related nephropathy through increasing mitochondrial biogenesis and activities.Journal of cellular and molecular medicine · 2020Article
- The Interplay of Renin-Angiotensin System and Toll-Like Receptor 4 in the Inflammation of Diabetic Nephropathy.Journal of immunology research · 2020Review
- Review
- Blockade of myeloid differentiation 2 attenuates diabetic nephropathy by reducing activation of the renin-angiotensin system in mouse kidneys.British journal of pharmacology · 2019Article
- Acetylshikonin from Zicao ameliorates renal dysfunction and fibrosis in diabetic mice by inhibiting TGF-β1/Smad pathway.Human cell · 2018Article
- A Network Pharmacology Approach to Uncover the Mechanisms of Shen-Qi-Di-Huang Decoction against Diabetic Nephropathy.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- "mTOR Signaling Pathway": A Potential Target of Curcumin in the Treatment of Spinal Cord Injury.BioMed research international · 2017Review
- Specific MAPK inhibitors prevent hyperglycemia-induced renal diseases in type 1 diabetic mouse model.Molecular and cellular biochemistry · 2016Article
- Calcitriol regulates angiotensin-converting enzyme and angiotensin converting-enzyme 2 in diabetic kidney disease.Molecular biology reports · 2016Article
- Epigenetic regulation of cardiac fibrosis.Journal of molecular and cellular cardiology · 2016Review
- Lycium barbarum Polysaccharide Mediated the Antidiabetic and Antinephritic Effects in Diet-Streptozotocin-Induced Diabetic Sprague Dawley Rats via Regulation of NF-κB.BioMed research international · 2016Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A range of in vitro, experimental and clinical intervention studies have implicated an important role for hyperglycaemia-induced activation of the renin-angiotensin system (RAS) in the development and progression of diabetic nephropathy (DN). Blockade of RAS by angiotensin converting enzyme (ACE) inhibitors is an effective strategy in treating diabetic kidney diseases. However, few studies demonstrate the mechanism by which hyperglycaemia up-regulates the expression of ACE gene. Our previous studies have identified a novel curcumin analogue, (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone (C66), which could inhibit the high glucose (HG)-induced phosphorylation of mitogen-activated protein kinases in mouse macrophages. In this study, we found that the renal protection of C66 in diabetic mice was associated with mitogen-activated protein kinase (MAPK) inactivation and ACE/angiotensin II (Ang II) down-regulation. Generally, MAPKs have been considered as a downstream signalling of Ang II and a mediator for Ang II-induced pathophysiological actions. However, using C66 and specific inhibitors as small molecule probes, in vitro experiments demonstrate that the MAPK signalling pathway regulates ACE expression under HG stimulation, which contributes to renal Ang II activation and the development of DN. This study indicates that C66 is a potential candidate of DN therapeutic agents, and more importantly, that reduction in ACE expression by MAPKs inhibition seems to be an alternative strategy for the treatment of DN.
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