Division of Nephrology, Taipei Veterans General Hospital
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Research Output

Publications

The TRTOI cohort has been published in leading nephrology journals.

2026

Epitranscriptomics in kidney disease: insights and therapeutic potential

Kidney Res Clin Pract. 2026 May;45(3):314-326.

Reviews how m⁶A RNA modification drives chronic kidney disease and renal fibrosis, highlighting it as a key molecular route regulating inflammation, metabolism and fibrosis. m⁶A RNA modification holds promise as a novel biomarker and precision therapeutic target in CKD, providing a foundation for emerging strategies such as RNA drugs and gene editing.

2026

Cell-Specific Roles of Angiopoietin-2 in CKD Collaborate with National Taiwan University Hospital using the TRTOI database

J Am Soc Nephrol. 2026 Apr 14. doi: 10.1681/ASN.0000001089.

This study establishes angiopoietin-2 as a key therapeutic target in CKD progression, with angiopoietin-2 from different cell sources playing distinct roles across disease stages, offering a new precision strategy. Angiopoietin-2 signaling could be inhibited in a stage-specific manner: blocking endothelial inflammation early and tubular fibrosis late to slow renal decline.

2026

Aldehyde dehydrogenase 2 mitigates acrolein-driven ferroptosis to preserve kidney function

Environ Pollut. 2026 Feb 1:390:127555.

This study shows that acrolein causes tubular injury by inducing mitochondrial dysfunction and ferroptosis, a mechanism aggravated by the ALDH2 Glu504Lys variant common in East Asians. Activating ALDH2 effectively reduces oxidative stress, restores mitochondrial function and mitigates kidney injury, suggesting ALDH2 activators as candidate precision CKD therapies for East Asian populations.

2024

Associations of urinary fetuin-A with histopathology and kidney events in biopsy-proven kidney disease

Clin Kidney J. 2024 Mar 14;17(4):sfae065.

This study identifies urinary fetuin-A as a key biomarker reflecting pathological injury and progression in CKD, able to predict renal decline and major adverse kidney events. The findings support building a non-invasive precision-medicine tool that improves risk assessment and clinical care in CKD.

2024

CXCL5 inhibition ameliorates acute kidney injury and prevents the progression from acute kidney injury to chronic kidney disease

Clin Sci (Lond). 2024 Nov 20;138(22):1451-1466.

This study identifies CXCL5 as a key driver of progression from acute kidney injury (AKI) to chronic kidney disease (CKD), accelerating renal decline through oxidative stress, inflammation and fibrosis. Inhibiting CXCL5 effectively reduces acute tubular injury and slows AKI-to-CKD progression, indicating its potential as a biomarker and novel therapeutic target.

2024

Aldehyde dehydrogenase 2 preserves kidney function by countering acrolein-induced metabolic and mitochondrial dysfunction

JCI Insight. 2024 Oct 8;9(19):e179871

This study clarifies how the ALDH2 variant common in East Asians promotes CKD progression and confirms the ALDH2–acrolein axis as a new therapeutic target. The findings provide an important scientific basis for precision CKD therapy and drug development for East Asian populations.

2024

Circulating Activin A, Kidney Fibrosis, and Adverse Events Best of ASN Journals 2024

Clin J Am Soc Nephrol (CJASN). 2024 Feb 1;19(2):169-177.

Analyzing 339 biopsy-confirmed TRTOI cohort patients, this study found plasma Activin A associated with tubulointerstitial fibrosis, renal INHBA expression and myofibroblasts, exploring its potential as a biomarker of kidney fibrosis.

2024

METTL3-Mediated N6-Methyladenosine mRNA Modification and cGAS-STING Pathway Activity in Kidney Fibrosis

J Am Soc Nephrol (JASN). 2024 Oct 1;35(10):1312-1329.

Analyzing 127 CKD specimens, this study found m6A modification and METTL3 expression markedly elevated, enhancing mRNA stability via the cGAS-STING pathway; tubule-specific Mettl3 knockout mice showed reduced inflammation and renal fibrosis.