ArticleBioscience reports2015
Fibrinogen-like protein 2 gene silencing inhibits cardiomyocytes apoptosis, improves heart function of streptozotocin-induced diabetes rats and the molecular mechanism involved.
Article in Bioscience reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Integrated meta-analysis and network pharmacology analysis: evaluation of Zhigancao decoction as treatment for diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Pooled it
- Potential clinical value of fibrinogen-like protein 1 as a serum biomarker for the identification of diabetic cardiomyopathy.Scientific reports · 2024Article
- Hydrogen sulfide plays an important role by regulating endoplasmic reticulum stress in myocardial diseases.Frontiers in pharmacology · 2023Review
- Gene expression profiles of rat MMECs with different glucose levels and fgl2 gene silencing.Diabetes/metabolism research and reviews · 2018Article
- FGL2 knockdown improves heart function through regulation of TLR9 signaling in the experimental autoimmune myocarditis rats.Immunologic research · 2018Article
- Adenovirus-mediated artificial miRNA targetting fibrinogen-like protein 2 attenuates the severity of acute pancreatitis in mice.Bioscience reports · 2017Article
- Increased expression of Fibrinogen-Like Protein 2 is associated with poor prognosis in patients with clear cell renal cell carcinoma.Scientific reports · 2017Article
- The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrinogen-like protein 2 (Fgl2) is involved in apoptosis, angiogenesis and inflammatory response. Diabetes is closely associated with apoptosis, angiogenesis and coagulation. So it allowed us to assume that Fgl2 plays an important role during the process of diabetic cardiomyopathy (DCM). In the present study, we test that the feasibility of Fgl2 as a therapeutic target for the treatment of DCM and its possible molecular mechanism involved. We found that Fgl2 gene silencing inhibits apoptosis and improves heart function of streptozotocin (STZ)-induced diabetes rats, the possible mechanism maybe that Fgl2 gene silencing reduces the tumour necrosis factor (TNF)±levels, decreases the expression of B-cell lymphoma-2 (bcl2), bcl-2-associated X (bax), toll-like receptors 4 (TLR4) and p38 mitogen-activated protein kinase (MAPK). In conclusion, Fgl2 is a potent target to treat DCM.
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