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Role of Neutrophil-derived HIF1a signaling in Hepatic Ischemia/Reperfusion Injury

Award Number: K01DK144335
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2031

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Role of Neutrophil-derived HIF1a signaling in Hepatic Ischemia/Reperfusion Injury - Project Summary Hepatic ischemia/reperfusion (I/R) injury is a leading cause of graft dysfunction following liver transplantation, which is the definitive therapeutic intervention for patients with end-stage liver disease. The use of marginal liver grafts, necessitated by the ongoing shortage of viable donors, further exacerbates post-transplant complications due to their increased susceptibility to I/R injury. However, the precise mechanisms underlying this pathological process remain inadequately characterized, impeding the development of effective therapies. Our preliminary findings from in vitro and in vivo studies, combined with results from single-cell RNA sequencing analysis, provide a strong foundation for our hypothesis that hypoxia-inducible factor (HIF)1a-induced macrophage migration inhibitory factor (MIF) in neutrophils exacerbates hepatic I/R injury by modulating macrophage-driven inflammation. We further hypothesize that targeting MIF could mitigate I/R injury. The primary objectives of this K01 proposal are to: 1) elucidate the mechanisms by which neutrophil-HIF1a/MIF contributes to I/R injury, 2) investigate therapeutic strategies targeting MIF, 3) acquire advanced expertise in liver innate immunity and I/R injury, which will be critical for achieving independence in liver pathology research, and 4) conduct proof-of- principle studies in patients undergoing liver transplantation. Upon completion of this proposed project, we expected to determine the regulation of MIF by neutrophil-derived HIF1a and its function in hepatic I/R injury (Aim 1), investigate the underlying mechanisms by which neutrophil-derived MIF exacerbates hepatic I/R injury (Aim 2), and evaluate the potential of targeting MIF to treat hepatic I/R injury (Aim 3). This K01 application will support the applicant's development into a highly skilled, independent principal investigator under the guidance of a Mentoring Committee comprised of accomplished scientists with well-established research teams and mentoring experience. The committee includes Dr. Cynthia Ju as primary mentor, Dr. Holger K Eltzschig as co- mentor, and Drs. Richard Bucala and Mark J Hobeika as key collaborators. They will provide full support for the proposed studies and oversee the applicant's career development. Upon completion of the project, the applicant will gain additional training to significantly advance expertise in HIF1a and MIF signaling, hepatic I/R injury, and liver inflammation. This strong foundation will enable further investigation of the therapeutic potential of targeting neutrophil-HIF1a/MIF signaling in other liver injuries and post-I/R repair, paving the way for a competitive R01 application and achieving his long-term career goal of becoming an independent investigator.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $158,220 )
2026	2026	UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER AT HOUSTON	7000 FANNIN ST FL 9	HOUSTON	TX	77030	HARRIS	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	5/4/2026	NEW	$158,220
														Subtotal = $158,220

Grand Total All Awards = $158,220

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Role of Neutrophil-derived HIF1a signaling in Hepatic Ischemia/Reperfusion Injury

Award Number: K01DK144335

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2031

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