Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

SUMOylation is a ubiquitin-related transient posttranslational modification pathway catalyzing the conjugation of small ubiquitin-like modifier (SUMO) proteins (SUMO1, SUMO2, and SUMO3) to lysine residues of proteins. SUMOylation targets a wide variety of cellular regulators and thereby affects a multitude of different cellular processes. SUMO/sentrin-specific proteases are able to remove SUMOs from targets, contributing to a tight control of SUMOylated proteins. Genetic and cell biological experiments indicate a critical role of balanced SUMOylation/deSUMOylation for proper cardiac development, metabolism, and stress adaptation. Here, we review the current knowledge about SUMOylation/deSUMOylation in the heart and provide an integrated picture of cardiac functions of the SUMO system under physiologic or pathologic conditions. We also describe potential therapeutic approaches targeting the SUMO machinery to combat heart disease.
...
PMID:The Ubiquitin-Like SUMO System and Heart Function: From Development to Disease. 2683 44

SUMOylation regulates diverse cellular processes including transcription, cell cycle, protein stability, and apoptosis. A recent research has now revealed the role of SUMO1 in cardiac disorders. Studies have evidenced that failing heart induces SUMO2/3 conjugation. Moreover, increased SUMO2/3- dependent modification has been observed to result in congestive heart disease such as cardiac hypertrophy by promoting cardiac cell death. Also, few recent studies have confirmed the role of SUMOylation in cardiac protein degradation. On the other hand, over-expression of SENP5, SUMO2/3-specific deconjugation enzyme has been observed to result in dilated cardiomyopathy or cardiac failure. So, the present review article would enlighten the latest updates about SUMOylation and associated factors during cardiac disorders.
 ...
PMID:SUMOylation in cardiac disorders - a review. 2842 47

Gestational zinc deficiency is a cause of congenital heart disease in the fetus, and sentrin/small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) as deSUMOylation enzymes play a crucial role in the development of cardiac structures. However, current studies of the regulation and function of SENP in zinc-deficient status during heart development remain limited. In this study, SUMO1 modification was found to gradually decrease during heart development, and the level of SENP5 exhibited a similar trend to SUMO1 conjugation. In addition, zinc deficiency resulted in cardiac dysplasia, increased cell apoptosis, decreased cell viability, and differentiation inhibition of hiPSC-CMs. In order to investigate the function of SENP5 in zinc deficiency, hiPSC-CMs were transfected with SENP5 small interfering RNA. The negative effects of zinc lacking conditions were reversed with depletion of SENP5. It was confirmed that zinc deficiency induced abnormal differentiation of hiPSCs and increased apoptosis of hiPSC-CMs by promoting SENP5 overexpression, which led to cardiac dysplasia. Thus, it was concluded that SENP5 regulates the SUMO1 deconjugation during heart development and zinc deficiency may reduce conjugated SUMO by promoting SENP5 overexpression, which induces abnormal development of the myocardium.
 ...
PMID:Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression. 3321 57