Words similar to hypertrophic
Example sentences for: hypertrophic
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Furthermore, persisting tension in the wound bed may explain why hypertrophic scars maintain the myofibroblast phenotype long after wound closure.
Iron deficiency has also been shown to lead to ventricular hypertrophy in developing rats [ 11 12 13 14 15 16 17 ] . While the mechanisms responsible for this hypertrophy have received little research attention, studies have documented an eccentric hypertrophic pattern [ 15 16 17 ] which has led investigators to suspect a ventricular volume overload at end diastole as a primary hypertrophic stimulus.
is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [ 8 ] . Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [ 9 10 11 ] . Control of thin filament length is critical for maintaining proper sarcomere function and length [ 12 ] . Inhibition of Tmod1's capping activity - either by using an antibody to its C-terminal end or by decreasing expression using an antisense Tmod1 transcript - results in elongated thin filaments and decreased cardiac contractility [ 13 14 ] . Tmod1 overexpression in rat cardiomyocytes causes shortening of the thin filaments and sarcomere disorganization, resulting in myofibril degeneration [ 14 ] . Likewise, mice overexpressing TMOD1 in the heart show disrupted sarcomere organization with shortened thin filaments, leading to myofibril degeneration and dilated cardiomyopathy [ 15 ] . Recently, Littlefield and colleagues showed that overexpression of GFP-Tmod1 in chick cardiac myocytes results in shortening of thin filaments; the authors proposed that excess Tmod1 decreases the affinity between actin monomers and pointed ends, leading to monomer dissociation and filament shortening [ 42 ] . Mutations in many proteins making up the cardiac sarcomere have been shown to cause cardiac hypertrophy [ 16 17 18 19 ] :mutations in the TPM1 gene, for example, cause type 3 familial hypertrophic cardiomyopathy (CMH3), and a transgenic mouse expressing a CMH3 mutation develops ventricular myocyte disarray and hypertrophy [ 20 ] . Mutations in myosin heavy chain 7 are estimated to account for 40-50% of the cases of hypertrophic cardiomyopathy [ 21 ] .
A loop present in the motor domain called the HCM (mutations in this loop cause hypertrophic cardiomyopathy) is the location of a phosphorylatable serine (S) or threonine (T) in certain amoeboid myosin I molecules and myosin VI molecules.
Comparisons of non-pressure vs. pressure-treated hypertrophic scars have shown that pressure supports the disappearance of α-SMA expressing myofibroblasts [ 54 ] . The data presented in this work suggest that body site differences in fibroblasts and wound tension are critical determinants of the keloid-less healing of palmoplantar wounds of keloid-prone individuals.
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