Skeletal muscle has attracted attention as endocrine organ, because exercise-dependent cytokines called myokines/exerkines are released from skeletal muscle and are involved in systemic functions. While, local mechanical loading to skeletal muscle by exercise or resistance training alters myofiber type and size and myonuclear number. Skeletal muscle-resident stem cells, known as muscle satellite cells (MuSCs), are responsible for the increased number of myonuclei. Under steady conditions, MuSCs are maintained in a mitotically quiescent state but exit from that state and start to proliferate in response to high physical activity. Alterations in MuSC behavior occur when myofibers are damaged, but the lethal damage to myofibers does not seem to evoke mechanical loading-dependent MuSC activation and proliferation. Given that MuSCs proliferate without damage, it is unclear how the different behaviors of MuSCs are controlled by different physical activities. Recent studies demonstrated that myonuclear number reflects the size of myofibers; hence, it is crucial to know the properties of MuSCs and the mechanism of myonuclear accretion by MuSCs. In addition, the elucidation of mechanical load-dependent changes in muscle resident cells, including MuSCs, will be necessary for the discovery of new myokines/exerkines and understating skeletal muscle diseases.
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J Korean Endocr Soc. 2007;22(1):11-18. Published online February 1, 2007
BACKGROUND A number of recent clinical studies have reported marked target organ damages in patients with primary aldosteronism. The aim of this study was to compare the incidence of target organ damages in patients with primary aldosteronism (PA) and essential hypertension (EHT). METHODS: The clinical records of 41 PA patients, over a 20-year period, were retrospectively analyzed. The clinical characteristics and incidence of target organ damages of 33 of the patients in this group were compared with those of 66 patients with essential hypertension, directly matched for age, gender and mean blood pressure. 8 of the PA patients could not be matched with EHT patients for age, gender and mean blood pressure, so were excluded from the comparison. The patients with essential hypertension were sampled from patients who visited for the evaluation of hypertension. RESULTS: Ischemic heart diseases were found in 18.2 and 10.6% of patients with PA and EHT, respectively (P = 0.22). From echocardiograms, left ventricular hypertrophy was found in 93.3% and 61.4% of patients with PA and EHT, respectively (P = 0.017). The degrees of left ventricular hypertrophy were correlated with the levels of serum aldosterone, with an r value of 0.490 (P < 0.005). Cerebrovascular attack was found in 18.2% and 1.5% of patients with PA and EHT, respectively (P = 0.005). Hypertensive retinopathy was found in 50% and 33.3% of patients with PA and EHT (P = 0.255), and nephropathy was found in 42.4% and 25.8% of patients with PA and EHT, respectively (P = 0.074). CONCLUSION: Patients with primary aldosteronism had target organ damages more frequently than with those with essential hypertension, which was independent of blood pressure.
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