• Journal of Periodontal and Implant Science
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• v.48 no.2
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• pp.92-102
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• 2018

Purpose: This study investigated the validity of the Charlson comorbidity index (CCI) as a predictor of periodontal disease (PD) over a 12-year period. Methods: Nationwide representative samples of 149,785 adults aged ${\geq}60$ years with PD (International Classification of Disease, 10th revision [ICD-10], K052-K056) were derived from the National Health Insurance Service-Elderly Cohort during 2002-2013. The degree of comorbidity was measured using the CCI (grade 0-6), including 17 diseases weighted on the basis of their association with mortality, and data were analyzed using multivariate Cox proportional-hazards regression in order to investigate the associations of comorbid diseases (CDs) with PD. Results: The multivariate Cox regression analysis with adjustment for sociodemographic factors (sex, age, household income, insurance status, residence area, and health status) and CDs (acute myocardial infarction, congestive heart failure, peripheral vascular disease, cerebral vascular accident, dementia, pulmonary disease, connective tissue disorders, peptic ulcer, liver disease, diabetes, diabetes complications, paraplegia, renal disease, cancer, metastatic cancer, severe liver disease, and human immunodeficiency virus [HIV]) showed that the CCI in elderly comorbid participants was significantly and positively correlated with the presence of PD (grade 1: hazard ratio [HR], 1.11; P<0.001; grade ${\geq}2$: HR, 1.12, P<0.001). Conclusions: We demonstrated that a higher CCI was a significant predictor of greater risk for PD in the South Korean elderly population.

• Journal of Animal Reproduction and Biotechnology
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• v.37 no.2
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• pp.67-79
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• 2022

Currently, there is no treatment to reverse or cure heart failure caused by ischemic heart disease and myocardial infarction despite the remarkable advances in modern medicine. In addition, there is a lack of evidence regarding the existence of stem cells involved in the proliferation and regeneration of cardiomyocytes in adult hearts. As an alternative solution to overcome this problem, protocols for differentiating human pluripotent stem cell (hPSC) into cardiomyocyte have been established, which further led to the development of cell therapy in major leading countries in this field. Recently, clinical studies have confirmed the safety of hPSC-derived cardiac progenitor cells (CPCs). Although several institutions have shown progress in their research on cell therapy using hPSC-derived cardiomyocytes, the functions of cardiomyocytes used for transplantation remain to be those of immature cardiomyocytes, which poses a risk of graft-induced arrhythmias in the early stage of transplantation. Over the last decade, research aimed at achieving maturation of immature cardiomyocytes, showing same characteristics as those of mature cardiomyocytes, has been actively conducted using various approaches at leading research institutes worldwide. However, challenges remain in technological development for effective generation of mature cardiomyocytes with the same properties as those present in the adult hearts. Therefore, in this review, we provide an overview of the technological development status for maturation methods of hPSC-derived cardiomyocytes and present a direction for future development of maturation techniques.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.4
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• pp.407-416
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• 2023

The regeneration of myocardium following acute circulatory events remains a challenge, despite numerous efforts. Mesenchymal stem cells (MSCs) present a promising cell therapy option, but their differentiation into cardiomyocytes is a time-consuming process. Although it has been demonstrated that PSME4 degrades acetyl-YAP1, the role of PSME4 in the cardiac commitment of MSCs has not been fully elucidated. Here we reported the novel role of PSME4 in MSCs cardiac commitment. It was found that overnight treatment with apicidin in primary-cultured mouse MSCs led to rapid cardiac commitment, while MSCs from PSME4 knock-out mice did not undergo this process. Cardiac commitment was also observed using lentivirus-mediated PSME4 knockdown in immortalized human MSCs. Immunofluorescence and Western blot experiments revealed that YAP1 persisted in the nucleus of PSME4 knockdown cells even after apicidin treatment. To investigate the importance of YAP1 removal, MSCs were treated with shYAP1 and apicidin simultaneously. This combined treatment resulted in rapid YAP1 elimination and accelerated cardiac commitment. However, overexpression of acetylation-resistant YAP1 in apicidin-treated MSCs impeded cardiac commitment. In addition to apicidin, the universal effect of histone deacetylase (HDAC) inhibition on cardiac commitment was confirmed using tubastatin A and HDAC6 siRNA. Collectively, this study demonstrates that PSME4 is crucial for promoting the cardiac commitment of MSCs. HDAC inhibition acetylates YAP1 and facilitates its translocation to the nucleus, where it is removed by PSME4, promoting cardiac commitment. The failure of YAP1 to translocate or be eliminated from the nucleus results in the MSCs' inability to undergo cardiac commitment.