• Biomolecules & Therapeutics
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• 제28권1호
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• pp.98-103
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• 2020

Marfan syndrome (MFS), a connective tissue disorder caused by mutations in the fibrillin-1 (Fbn1) gene, has vascular manifestations including aortic aneurysm, dissection, and rupture. Its vascular pathogenesis is assumed to be attributed to increased transforming growth factor β (TGFβ) signaling and blockade of excessive TGFβ signaling has been thought to prevent dissection and aneurysm formation. Here, we investigated whether galunisertib, a potent small-molecule inhibitor of TGFβ receptor I (TβRI), attenuates aneurysmal disease in a murine model of MFS (Fbn1^C1039G/+) and compared the impact of galuninsertib on the MFS-related vascular pathogenesis with that of losartan, a prophylactic agent routinely used for patients with MFS. Fbn1^C1039G/+ mice were administered galunisertib or losartan for 8 weeks, and their ascending aortas were assessed for histopathological changes and phosphorylation of Smad2 and extracellular signal-regulated kinase 1/2 (Erk1/2). Mice treated with galunisertib or losartan barely exhibited phosphorylated Smad2, suggesting that both drugs effectively blocked overactivated canonical TGFβ signaling in Fbn1^C1039G/+ mice. However, galunisertib treatment did not attenuate disrupted medial wall architecture and only partially decreased Erk1/2 phosphorylation, whereas losartan significantly inhibited MFS-associated aortopathy and markedly decreased Erk1/2 phosphorylation in Fbn1^C1039G/+ mice. These data unexpectedly revealed that galunisertib, a TβRI inhibitor, showed no benefits in aneurysmal disease in MFS mice although it completely blocked Smad2 phosphorylation. The significant losartan-induced inhibition of both aortic vascular pathogenesis and Smad2 phosphorylation implied that canonical TGFβ signaling might not prominently drive aneurysmal diseases in MFS mice.

• 운동영양학회지
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• 제25권2호
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• pp.1-7
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• 2021

[Purpose] Recent studies have shown that COVID-19 is often associated with altered gut microbiota composition and reflects disease severity. Furthermore, various reports suggest that the interaction between COVID-19 and host-microbiota homeostasis is mediated through the modulation of microRNAs (miRNAs). Thus, in this review, we aim to summarize the association between human microbiota and miRNAs in COVID-19 pathogenesis. [Methods] We searched for the existing literature using the keywords such "COVID-19 or microbiota," "microbiota or microRNA," and "COVID-19 or probiotics" in PubMed until March 31, 2021. Subsequently, we thoroughly reviewed the articles related to microbiota and miRNAs in COVID-19 to generate a comprehensive picture depicting the association between human microbiota and microRNAs in the pathogenesis of COVID-19. [Results] There exists strong experimental evidence suggesting that the composition and diversity of human microbiota are altered in COVID-19 patients, implicating a bidirectional association between the respiratory and gastrointestinal tracts. In addition, SARS-CoV-2 encoded miRNAs and host cellular microRNAs modulated by human microbiota can interfere with viral replication and regulate host gene expression involved in the initiation and progression of COVID-19. These findings suggest that the manipulation of human microbiota with probiotics may play a significant role against SARS-CoV-2 infection by enhancing the host immune system and lowering the inflammatory status. [Conclusion] The human microbiota-miRNA axis can be used as a therapeutic approach for COVID-19. Hence, further studies are needed to investigate the exact molecular mechanisms underlying the regulation of miRNA expression in human microbiota and how these miRNA profiles mediate viral infection through host-microbe interactions.

• Molecules and Cells
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• 제46권4호
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• pp.191-199
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• 2023

The Golgi apparatus modifies and transports secretory and membrane proteins. In some instances, the production of secretory and membrane proteins exceeds the capacity of the Golgi apparatus, including vesicle trafficking and the post-translational modification of macromolecules. These proteins are not modified or delivered appropriately due to the insufficiency in the Golgi function. These conditions disturb Golgi homeostasis and induce a cellular condition known as Golgi stress, causing cells to activate the 'Golgi stress response,' which is a homeostatic process to increase the capacity of the Golgi based on cellular requirements. Since the Golgi functions are diverse, several response pathways involving TFE3, HSP47, CREB3, proteoglycan, mucin, MAPK/ETS, and PERK regulate the capacity of each Golgi function separately. Understanding the Golgi stress response is crucial for revealing the mechanisms underlying Golgi dynamics and its effect on human health because many signaling molecules are related to diseases, ranging from viral infections to fatal neurodegenerative diseases. Therefore, it is valuable to summarize and investigate the mechanisms underlying Golgi stress response in disease pathogenesis, as they may contribute to developing novel therapeutic strategies. In this review, we investigate the perturbations and stress signaling of the Golgi, as well as the therapeutic potentials of new strategies for treating Golgi stress-associated diseases.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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• pp.29-34
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• 2003

Visceral fat accumulation is known to be an evident clinical index for the insulin resistance related with obesity. Patients with excessive accumulation of visceral fat frequently suffered from metabolic disorder, such as hyperlipidemia, hypertension, and glucose intolerance. However, molecular mechanism for the pathogenesis of obesity-accompanied metabolic disorders has not been fully elucidated. It has been clarified that adipocytes in visceral fat area have different functions from subcutaneous fat area, and these differences might contribute the pathological significance of excessive accumulation of visceral fat for the accompanied insulin resistance and hyperinsulinemia.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2000년도 한국생물과학협회 학술발표대회
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• pp.269.2-269
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• 2000

No Abstract, See Full Text

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2002년도 제9회 학술 발표회 프로그램과 논문초록
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• pp.29-29
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• 2002

In response to fungal invasion and other signals, plants accumulate a number of proteins that are involved in defense against pathogens. Osmotin is a 24 kDa protein belonging to the pathogenesis-related (PR) protein, a component of the hypersensitive response in leaves of tobacco plants exposed to tobacco mosaic virus.(omitted)

• 한국동물학회:학술대회논문집
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• 한국동물학회 2003년도 한국생물과학협회 학술발표대회
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• pp.25-25
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• 2003

No Abstract, See Full Text

• 대한유전성대사질환학회지
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• 제5권1호
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• pp.76-87
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• 2005

Various disorders cause hyperammonemia during childhood. Amongthem are those caused by inherited defects in urea synthesis and related metabolic pathways. These disorders can be grouped into two types: disorders of the enzymes that comprise the urea cycle, and disorders of the transporters or metabolites of theamino acids related to the urea cycle. Principal clinical features of these disorders are caused by elevated levels of blood ammonium. Additional disease-specific symptoms are related to the particular metabolic defect. These specific clinical manifestations are often due to an excess or lack of specific amino acids. Treatment of urea cycle disorders and related metabolic diseases consists of nutritional restriction of proteins, administration of specific amino acids, and use of alternative pathways for discarding excess nitrogen. Although combinations of these treatments are extensively employed, the prognosis of severe cases remains unsatisfactory. Liver transplantation is one alternative for which a better prognosis is reported.

• 동의생리병리학회지
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• 제16권5호
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• pp.857-866
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• 2002

The main current in the pathology of oriental medicine is composed of etiologic factor, pathogenesis and clinical manifestation. The access of a disease is consist of etiologic factor, location of the lesion, nature of the disease and patient's condition. The nature of disease and the property of a drug are inseparably related to each other. The nature of disease is composed of six exogenous factors, cold and heat, deficiendy and excess, Yinyang and pain. Cold nature is divided into cold symptom due to excess and asthenia cold, fever nature is divided into sthenic fever and asthenic fever. According to the location, cold and heat can be subdivided into heat in the upper and cold in the lower, cold in the upper and heat in the lower, exterior cold and interior heat, exterior heat and interior cold. Yin syndrome characterized by hypofunction of the viscera is generated from insufficiency of yang-qi, excess of yin-coldness, deficiency of both qi and the blood.

• 동의생리병리학회지
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• 제16권5호
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• pp.831-839
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• 2002

Allergy has a born predominant cause of atopy in body and react oversenstively several meterial. The cause of allergy are tick, house dust, egg, milk, bean, cosmetics, virus, bacteria, flesh and meat in Western medicine. While, Oriental medicine did not have an application on the allergy, but recognized that allergy is connected with fetal toxicosis, heat-syndrome in new born, syndrome characterized by dyspnea, sneezing, stuffy nose, nasal discharge and phlegm. Therefor, We knowed method of medical treatment following cause of disease and pathogenesis against allergy. Allergic disease(atopic dermatitis, bronchial asthma, rhinitis) were related with lung, spleen, kidney. To prevent allergic disease in born, Oriental medicine taked a serious view of fetal education. In Western medicine, The cause of allergy applied to exopathogen of Oriental medicine. In Oriental medicine, Treatment of allergy used generally strengthening the body resistance to eliminate pathogenic factors.