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Jih-Yang Ko

Researcher at Chang Gung University

Publications -  128
Citations -  3545

Jih-Yang Ko is an academic researcher from Chang Gung University. The author has contributed to research in topics: Osteoarthritis & Rotator cuff. The author has an hindex of 33, co-authored 113 publications receiving 2932 citations. Previous affiliations of Jih-Yang Ko include Memorial Hospital of South Bend.

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Modulation of Dickkopf-1 Attenuates Glucocorticoid Induction of Osteoblast Apoptosis, Adipocytic Differentiation, and Bone Mass Loss

TL;DR: Interference with the osteogenesis-inhibitory action of DKK1 has therapeutic potential for preventing glucocorticoid induction of osteopenia and appeared to protect bone tissue by modulating beta-catenin and Akt-mediated survival as well as the osteogenic and adipogenic activities of glucose-stressed osteoprogenitor cells.
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MicroRNA-29a Promotion of Nephrin Acetylation Ameliorates Hyperglycemia-Induced Podocyte Dysfunction

TL;DR: Hyperglycemia impairs miR-29a signaling to intensify HDAC4 actions that contribute to podocyte protein deacetylation and degradation as well as renal dysfunction, which highlights the importance of post-translational acetylation reactions in podocyte microenvironments.
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Extracorporeal Shockwave for Chronic Patellar Tendinopathy

TL;DR: Extracorporeal shockwave therapy appeared to be more effective and safer than traditional conservative treatments in the management of patients with chronic patellar tendinopathy.
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Control of Dkk-1 ameliorates chondrocyte apoptosis, cartilage destruction, and subchondral bone deterioration in osteoarthritic knees.

TL;DR: Interference with the cartilage- and bone-deleterious actions of Dkk-1 provides therapeutic potential for alleviating cartilage destruction and subchondral bone damage in OA knee joints.
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MicroRNA‐29a Protects Against Glucocorticoid‐Induced Bone Loss and Fragility in Rats by Orchestrating Bone Acquisition and Resorption

TL;DR: Promotion of miR-29a signaling is an alternative strategy for alleviating glucocorticoid-induced bone deterioration and improved osteoblast differentiation and mineral acquisition.