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Frank Y. Ma

Researcher at Monash Medical Centre

Publications -  56
Citations -  2632

Frank Y. Ma is an academic researcher from Monash Medical Centre. The author has contributed to research in topics: Kidney & Renal fibrosis. The author has an hindex of 29, co-authored 54 publications receiving 2196 citations. Previous affiliations of Frank Y. Ma include University of Otago & Royal Children's Hospital.

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Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db / db mice

TL;DR: It is demonstrated that MCP-1 promotes type 2 diabetic renal injury but does not influence the development of obesity, insulin resistance or type 2 diabetes in db/db mice.
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TGF-β/Smad3 signalling regulates the transition of bone marrow-derived macrophages into myofibroblasts during tissue fibrosis

TL;DR: It is demonstrated that bone marrow-derived fibroblasts originate from the monocyte/macrophage population via a process of MMT, which contributes to progressive renal tissue fibrosis and is regulated by TGF-β/Smad3 signalling.
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The JNK Signaling Pathway in Renal Fibrosis

TL;DR: In conclusion, JNK signaling plays an integral role in several key mechanisms operating in renal fibrosis, and targeting of JNK enzymes has therapeutic potential for the treatment of fibrotic kidney diseases.
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A Pathogenic Role for c-Jun Amino-Terminal Kinase Signaling in Renal Fibrosis and Tubular Cell Apoptosis

TL;DR: This is the first study to demonstrate that JNK signaling plays a pathogenic role in renal fibrosis and tubular apoptosis, and JNK1 plays a nonredundant role in tubular cell apoptosis.
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TGF-β1-activated kinase-1 regulates inflammation and fibrosis in the obstructed kidney.

TL;DR: TAK1 is established as a major upstream activator of JNK, p38, and NF-κB signaling in the obstructed kidney, and they define a pathologic role for TAK1 in renal inflammation and fibrosis.