Kim Jun-Dal

Associate Professor

University of Toyama

Japan

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Kim Jun-Dal is an Associate Professor at the University of Toyama, Japan. His research primarily focuses on neural stem cells, inflammatory responses to aging, and various aspects of renal and cardiac physiology. Recent publications highlight his work on the impacts of metabolic changes in disease states, as well as the exploration of treatment effects on conditions like pulmonary hypertension and Alzheimer's disease.

Articles (15)

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2025

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2025

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2025

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2024

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2023

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2023

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2022

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2022

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2021

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2021

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2021

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2021

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Professor

University of Toyama

JAPAN

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Kim Jun-Dal

Research Interests

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Articles (15)

Neural stem cell-specific deficiency of (pro)renin receptor causes brain malformation and perinatal lethality in mice.

Protein arginine methylation regulates anti-inflammatory programming in response to aging stress.

A novel glomerulopathy model demonstrates renal counterbalance via local angiotensin II regulation.

Impact of the SIK3 Pathway Inhibition on Osteoclast Differentiation via Oxidative Phosphorylation

Deciphering the inhibitory effects of trimetazidine on pulmonary hypertension development via decreasing fatty acid oxidation and promoting glucose oxidation.

Metabolic changes in the plasma of mild Alzheimer’s disease patients treated with Hachimijiogan

Increased angiotensin II coupled with decreased Adra1a expression enhances cardiac hypertrophy in pregnancy-associated hypertensive mice.

Multi‑omics analysis of right ventricles in rat models of pulmonary arterial hypertension: Consideration of mitochondrial biogenesis by chrysin

Wogonin, a Compound in Scutellaria baicalensis, Activates ATF4–FGF21 Signaling in Mouse Hepatocyte AML12 Cells

Pathophysiological Roles of Stress-Activated Protein Kinases in Pulmonary Fibrosis

Temporal transcriptomic profiling reveals dynamic changes in gene expression of Xenopus animal cap upon activin treatment.

Starvation‐induced transcription factor CREBH negatively governs body growth by controlling GH signaling

Disruption of entire Cables2 locus leads to embryonic lethality by diminished Rps21 gene expression and enhanced p53 pathway.

Transcriptomic Evaluation of Pulmonary Fibrosis-Related Genes: Utilization of Transgenic Mice with Modifying p38 Signal in the Lungs.

Loss of PRMT1 in the central nervous system (CNS) induces reactive astrocytes and microglia during postnatal brain development.

Collaborators (6)

Kazuya Murata

Kowit Hengphasatporn

Takashi Nakagawa

Tomoyuki KUWAKI

Yoshitoshi Kasuya

Yoshimi Nakagawa

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