K
Kyung Hwan Kim
Researcher at Yonsei University
Publications - 192
Citations - 4550
Kyung Hwan Kim is an academic researcher from Yonsei University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 37, co-authored 162 publications receiving 4056 citations. Previous affiliations of Kyung Hwan Kim include KAIST & Seoul National University Hospital.
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Journal ArticleDOI
Pathogenesis of diabetic nephropathy: the role of oxidative stress and protein kinase C
Hunjoo Ha,Kyung Hwan Kim +1 more
TL;DR: Proposed mechanisms involved in oxidative stress associated with hyperglycemia are glucose autooxidation, the formation of advanced glycosylation end products, and metabolic stress resulting from hyperglycesmia.
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Nuclear factor-kappaB regulates cyclooxygenase-2 expression and cell proliferation in human gastric cancer cells.
TL;DR: NF-κB mediates COX-2 expression, which may be related to cell proliferation, in human gastric cancer cells, in a dose-dependant manner.
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Transporter-mediated bile acid uptake causes Ca2+-dependent cell death in rat pancreatic acinar cells.
Joo Young Kim,Kyung Hwan Kim,Jin Ah Lee,Wan Namkung,An–Qiang Sun,Meena Ananthanarayanan,Frederick J. Suchy,Dong Min Shin,Shmuel Muallem,Min Goo Lee +9 more
TL;DR: It is suggested that bile acids can be transported into pancreatic acinar cells through specific membrane transporters and induce cell death by impairing cellular Ca(2+) signaling.
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Melatonin and taurine reduce early glomerulopathy in diabetic rats.
TL;DR: Beneficial effects of melatonin and taurine are demonstrated on early changes in diabetic kidney and suggest that diabetic nephropathy associated with hyperglycemia is largely mediated by oxidative stress.
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Dna damage in the kidneys of diabetic rats exhibiting microalbuminuria
TL;DR: Daily injection of insulin starting on the third day after streptozotocin treatment significantly reduced both urinary albumin excretion and papillary 8-OHdG formation, which suggests that these are associated with the diabetic state induced by streptoocin rather than a direct nephrotoxic effect of the drug.