Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q9UID6 (Kruppel-like)
 147 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac hypertrophy is considered an early hallmark during the clinical course of heart failure and an important risk factor for cardiac morbidity and mortality. Although hypertrophy of individual cardiomyocytes in response to pathological stimuli has traditionally been considered as an adaptive response required to sustain cardiac output, accumulating evidence from studies in patients and animal models suggests that in most instances hypertrophy of the heart also harbors maladaptive aspects. Major strides have been made in our understanding of the pathways that convey pro-hypertrophic signals from the outside of the cell to the nucleus. In recent years it also has become increasingly evident that the heart possesses a variety of endogenous feedback mechanisms to counterbalance this growth response. These repressive mechanisms are of particular interest since they may provide valuable therapeutic options. In this review we summarize currently known endogenous repressors of pathological cardiac growth as they have been studied by gene targeting in mice. Many of the repressors that function in signal transduction appear to regulate calcineurin (e.g. PICOT, calsarcin, RCAN) and JNK signaling (e.g. CDC42, MKP-1) and some will be described in greater detail in this review. In addition, we will focus on factors such as Kruppel-like factors (KLF4, KLF15 and KLF10) and histone deacetylases (HDACs), which constitute a relevant group of nuclear proteins that repress transcription of the hypertrophic gene program in cardiomyocytes.
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PMID:Tapping the brake on cardiac growth-endogenous repressors of hypertrophic signaling. 2158 93

Kruppel-like factor 15 (KLF15) is a subtype of the Kruppel-like family of transcription factors (KLFs). KLFs have three high-fidelity zinc fingers at the carboxyl terminus that enable them to regulate the biological processes of proliferation, differentiation, cellular development, and apoptosis. KLF15 is highly expressed in the kidney, pancreas, and cardiac and skeletal muscle, and plays an essential role in the development and occurrence of multiple system diseases. In this paper, we underscored the important relationship between KLF15 and cardiovascular diseases such as atherosclerosis, heart failure, arrhythmia, aortic lesions, etc. On this basis, we identified KLF15 as a potential therapeutic target for the treatment of cardiovascular disease.
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PMID:Advances in the relationship between Kruppel-like factor 15 and cardiovascular disease research. 3164 78