Publications
21
Citations
424
Est. group size
~7
Recurring co-author estimate
Active years
14
Publishing since 2013
This researcher studies how cells communicate and die in disease, with work spanning liver fibrosis (scarring), heart failure after heart attacks, and tuberculosis infection. A recurring theme is the protein CEACAM1 and its role in liver disease, alongside studies of immune cell trafficking via extracellular vesicles (tiny cell-released particles) and mitochondrial function in infection and metabolic disease. Prospective students would likely engage with lab-based experimental work using cell and animal models to understand disease mechanisms at the molecular level.
Publication output has grown over the last decade, rising from occasional single papers in the late 2010s to a steadier average of about 3 per year in the last 5 years, with a notable increase in 2024-2025.
Generated by claude-sonnet-5 from public bibliographic data · Jul 20, 2026
- Extracellular Vesicles Mediate Activation and Trafficking of Splenic Immune Cells to the Heart Post-Myocardial Infarction
bioRxiv (Cold Spring Harbor Laboratory) · 2026
- Diminished CEACAM1 level plays a critical role in age-related hepatic fibrosis
Mechanisms of Ageing and Development · 2025
- Extracellular Vesicles Mediate Splenic Immune Activation and Trafficking to the Heart post-Myocardial Infarction
Physiology · 2025
- Loss of <scp>CEACAM1</scp> in hepatocytes causes hepatic fibrosis
European Journal of Clinical Investigation · 2024
- Conditional deletion of CEACAM1 in hepatic stellate cells causes their activation
Molecular Metabolism · 2024
- Rv0547c, a functional oxidoreductase, supports Mycobacterium tuberculosis persistence by reprogramming host mitochondrial fatty acid metabolism
Mitochondrion · 2024
- Conditional deletion of CEACAM1 causes hepatic stellate cell activation
bioRxiv (Cold Spring Harbor Laboratory) · 2024
- Exosomes mediate immune activation post-myocardial infarction
Physiology · 2023
- TNFR1 Contributes to Activation-Induced Cell Death of Pathological CD4+ T Lymphocytes During Ischemic Heart Failure
JACC Basic to Translational Science · 2022
- TNFR1 Contributes to Activation Induced Cell Death of Pathological Cd4+ T-Lymphocytes During Ischemic Heart Failure
SSRN Electronic Journal · 2022
- Abstract P3068: TNFR1 Regulates Cellular Proliferation And Not Pathogenicity Of Cd4 <sup>+</sup> T-lymphocytes During Ischemic Heart Failure
Circulation Research · 2022
- Regulation of hepatic fibrosis by carcinoembryonic antigen-related cell adhesion molecule 1
Metabolism · 2021
- Nicotinamide Mononucleotide Prevents Free Fatty Acid-Induced Reduction in Glucose Tolerance by Decreasing Insulin Clearance
International Journal of Molecular Sciences · 2021
- Cell death at the cross roads of host-pathogen interaction in Mycobacterium tuberculosis infection
Tuberculosis · 2018
- Small Molecule Mediated Restoration of Mitochondrial Function Augments Anti-Mycobacterial Activity of Human Macrophages Subjected to Cholesterol Induced Asymptomatic Dyslipidemia
Frontiers in Cellular and Infection Microbiology · 2017
- bioRxiv (Cold Spring Harbor Laboratory)×2
- Physiology×2
- Tuberculosis×1
- JACC Basic to Translational Science×1
- Scientific Reports×1
- Wenjun Zhang
Medicine · Indiana University
- Wencheng Zhang
Medicine · Purdue University West Lafayette
- Mauricio Rojas
Medicine · The Ohio State University
- Alexa Petrucciani
Medicine · Purdue University West Lafayette
- Adrian Gardner
Medicine · Indiana University
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 19, 2026.
Claim or correct this profile