Haberzettl Lab
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About
Our team aims to understand how environmental exposures impair cardiovascular and metabolic function in healthy and susceptible individuals. Goal of our ongoing research is to determine the mechanisms by which exposures to polluted air increases the risk of developing cardiovascular disease and type-2 diabetes and how susceptible states such as obesity, circadian misalignment, or advanced age predispose individuals to air pollution toxicity. Additional projects investigate how circadian and sleep alterations induced by environmental exposures contribute to the development of cardiometabolic disease. In this context we investigate how exposure to non-traditional and traditional environmental factors impact sleep, circadian rhythm and cardiometabolic health. Our research encompasses the following questions:
How does exposure to traditional or non-traditional environmental factors such as air and light pollution impact cardiovascular and metabolic health?
Which are groups that are more susceptible to environmental exposures? and What mechanism(s) are involved that triggering these sensitivities?
Which are the signaling pathways induced by environmental stressors that contribute to the development of cardiometabolic disease?
Team
Amanda C. Ribble, B.S., amanda.ribble@louisville.edu
Key Research Areas
Air pollution
Cardiovascular Disease (CVD)
Chronotoxicity
Circadian Rhythm
Inflammation
Insulin Resistance
Light pollution
Sleep
Type-2 diabetes (T2D)
Vascular Injury & Repair
Selected Publications
- Haberzettl, P., … (2018). Endothelial progenitor cells: Properties, function, and response to toxicological stimuli. In C. A. MacQueen (Ed.), Comprehensive toxicology. Elsevier.
- Haberzettl, P., … (2014). Particulate matter and oxidative stress – Pulmonary and cardiovascular targets and consequences. In I. Laher (Ed.), Systems biology of free radicals and antioxidants. Springer.
- Kitching, M., … Haberzettl, P. (2025). Sex differences in the redox response to fine particulate matter (PM2.5) air pollution protects female mice against metabolic and cardiac injury. Physiological Reports, 13(17), e70536. https://pubmed.ncbi.nlm.nih.gov/40892707/
- Gomes, D., … Haberzettl, P. (2025). Inhalation of concentrated ambient PM2.5 promotes inactivation of telomerase reverse transcriptase, telomere shortening, and senescence of multiple cell types in mice. Toxicological Sciences, 206(1), 147–157. https://pubmed.ncbi.nlm.nih.gov/40172909/
- Asplund, H., … Haberzettl, P. (2024). Exposure to fine particulate matter air pollution disrupts erythrocyte turnover. Circulation Research, 134, 1224–1227. https://pubmed.ncbi.nlm.nih.gov/38662858/
- Ribble, A., … Haberzettl, P. (2023). Fine particulate matter (PM2.5)-induced pulmonary oxidative stress contributes to increases in glucose intolerance and insulin resistance in a mouse model of circadian dyssynchrony. Science of the Total Environment, 877, 162934. https://pubmed.ncbi.nlm.nih.gov/36934930/
- Kurlawala, Z., … Haberzettl, P. (2023). Fine particulate matter (PM2.5)-induced pulmonary oxidative stress contributes to changes in the plasma lipidome and liver transcriptome in mice. Toxicological Sciences, 192(2), 209–222. https://pubmed.ncbi.nlm.nih.gov/36857595/
- Hill, B. G., … Haberzettl, P. (2021). Fine particulate matter (PM2.5) inhalation-induced alterations in the plasma lipidome as promoters of vascular inflammation and insulin resistance. American Journal of Physiology-Heart and Circulatory Physiology, 320(5), H1836–H1850. https://pubmed.ncbi.nlm.nih.gov/33666505/
- Singh, P., … Haberzettl, P. (2021). Endothelial progenitor cells as critical mediators of environmental air pollution-induced cardiovascular toxicity. American Journal of Physiology-Heart and Circulatory Physiology, 320(4), H1440–H1455. https://pubmed.ncbi.nlm.nih.gov/33606580/
- Haberzettl, P. (2018). Circadian toxicity of environmental pollution: Inhalation of polluted air to give a precedent. Current Opinion in Physiology, 16–24. https://pubmed.ncbi.nlm.nih.gov/30931418/
- Haberzettl, P., … (2018). Inhalation of fine particulate matter impairs endothelial progenitor cell function via pulmonary oxidative stress. Arteriosclerosis, Thrombosis, and Vascular Biology, 38(1), 131–142. https://pubmed.ncbi.nlm.nih.gov/29191925/
- Haberzettl, P., … (2016). Exposure to fine particulate air pollution causes vascular insulin resistance by inducing pulmonary oxidative stress. Environmental Health Perspectives, 124(12), 1830–1839. https://pubmed.ncbi.nlm.nih.gov/27128347/
- Haberzettl, P., … (2016). Insulin sensitizers prevent fine particulate matter-induced vascular insulin resistance and changes in endothelial progenitor cell homeostasis. American Journal of Physiology-Heart and Circulatory Physiology, 310(11), H1423–H1438. https://pubmed.ncbi.nlm.nih.gov/27016579/
- Haberzettl, P., … (2012). Exposure to ambient air fine particulate matter prevents VEGF-induced mobilization of endothelial progenitor cells from the bone marrow. Environmental Health Perspectives, 120(6), 848–856. https://pubmed.ncbi.nlm.nih.gov/22418586/