About

Professor Fadi Khasawneh is associated with the Irma Lerma Rangel College of Pharmacy at Texas A&M University. The provided page text does not include specific details about his research focus, background, or key contributions. The content primarily discusses the college's initiatives to support first-generation students and shares personal stories of first-generation students, including the founding dean, Indra K. Reddy, PhD. Therefore, there is no detailed biographical or research information available for Professor Fadi Khasawneh in the provided text.

Research topics

• Internal medicine
• Medicine
• Immunology
• Biology
• Cell biology
• Pathology
• Cardiology

Selected publications

• Low dose thirdhand smoke exposure enhances platelet functional responses in mice

  Experimental Biology and Medicine · 2026-03-12

  articleOpen accessSenior author

  Although cigarette smoking is the most preventable cause of cardiovascular diseases, most researchers have focused on either direct/firsthand or secondhand smoke exposures. Recently though, attention has shifted to an emerging/indirect exposure trend-known as thirdhand smoke (THS)- which was previously “overlooked.” This phenomenon, which was/is thought to be harmless, has been identified as a serious health risk, including in the context of thrombogenesis/platelets. However, whether low dose THS exposure has the capacity to modulate platelets has not been investigated. Two sets of household materials were exposed to 20 cigarettes/day for a week on an alternating basis, with controls exposed to clean air. After the first set of exposed materials is placed in mice cages, exposure of the second set is initiated. The materials were interchanged weekly, for a total exposure duration of 1 month. Mice were then subjected to multiple platelet function assays. THS exposed mice exhibited shortened tail bleeding and occlusion times, indicating a prothrombotic phenotype. Moreover, we also observed that platelets from the exposed mice exhibited an enhanced aggregation response. However, we did not observe any gender differences in our in vivo as well as aggregation experiments; hence, subsequent characterization was carried out on male mice. It was also found that dense granules release, integrin activation, and PS exposure were also potentiated in the exposed platelets compared to the controls. Finally, we observed for the first time that the tobacco-specific nitrosamine and THS toxicant NNK enhanced platelet aggregation and thrombus formation. Collectively, we provide documentation that low dose of THS exposure is detrimental to health by increasing the risk of thrombosis through a hyperactive platelet phenotype that involves the toxicant NNK.

  PublisherOA PDFDOI

• The Prothrombotic Phenotype of Thirdhand Electronic Cigarette Exposure is Sex Independent and Involves Systemic Mediated Effects on Platelet Function: Evidence from a Mouse Model

  Cardiovascular Toxicology · 2026-02-17

  articleOpen access

  Electronic cigarettes (e-cigs) are major contributors to inflammatory-mediated responses, which are implicated in a vast array of pathophysiological conditions, including cardiovascular disease (CVD). More recently e-cigs have been recognized as a source of thirdhand exposure (THEC); the process by which expelled toxins settle on materials (i.e., carpets, curtains, clothes etc.) and undergo chemical reactions, rendering them more harmful overtime. Herein, mice were exposed to THEC for four months, and platelet reactivity, systemic mediated effects on platelet function, and cytokine expression profiles were analyzed in both sexes. Our data revealed a hyperactive platelet phenotype as determined by shortened bleeding and occlusion times, enhanced platelet aggregation, and dense granule secretion with no significant difference between males and females. Cytokines, amongst other inflammatory molecules, are well documented mediators by which platelet function is modulated and they also enhance susceptibility to CVD. To this end, and to elucidate the mechanism by which platelet reactivity was augmented, washed platelets that were exposed only to clean air (CA) and resuspended in THEC exposed plasma, displayed significantly increased platelet aggregation, dense granule secretion, and p-selectin expression. Indeed, this data suggests that THEC exposure elicits a systemic effect, enhancing platelet response, and was further validated by a dysregulated cytokine profile using plasma, free of platelets, in a sex-dependent manner. Collectively and for the first time, we highlight that both males and females are at similar risk of THEC-mediated prothrombotic phenotype, which is underlined-at least in part- by an indirect systemic effect of exposure on platelet reactivity that involves changes in the cytokine profile. These findings underscore this form of exposure as a threat to cardiovascular health.

  PublisherOA PDFDOI

• The Platelet Regulator of G-Protein Signaling 16 Negatively Regulates Platelet Function (Abstract ID: 235189)

  Journal of Pharmacology and Experimental Therapeutics · 2026-05-01

  articleSenior author
  PublisherDOI

• Pyroptosis of pulmonary fibroblasts and macrophages through NLRC4 inflammasome leads to acute respiratory failure

  Cell Reports · 2025-03-31 · 11 citations

  articleOpen access

  The NAIP/NLRC4 inflammasome plays a pivotal role in the defense against bacterial infections, with its in vivo physiological function primarily recognized as driving inflammation in immune cells. Acute lung injury (ALI) is a leading cause of mortality in sepsis. In this study, we identify that the NAIP/NLRC4 inflammasome is highly expressed in both macrophages and pulmonary fibroblasts and that pyroptosis of these cells plays a critical role in lung injury. Mice challenged with gram-negative bacteria or flagellin developed lethal lung injury, characterized by reduced blood oxygen saturation, disrupted lung barrier function, and escalated inflammation. Flagellin-induced lung injury was protected in caspase-1 or GSDMD-deficient mice. These findings enhance our understanding of the NAIP/NLRC4 inflammasome's (patho)physiological function and highlight the significant role of inflammasome activation and pyroptosis in ALI during sepsis.

  PublisherOA PDFDOI

• BNP promotes platelet activation and thrombosis via its receptor natriureticpeptide receptor-a (NPRA): A paradigm shift from biomarker to effector

  Blood · 2025-11-03

  articleOpen access

  Abstract Background-B-type natriuretic peptide (BNP) is a cardiac-derived vasodilator and a well-established biomarker for heart failure. Elevated BNP and its cleavage product N-terminal proBNP (NT-proBNP) also predict adverse outcomes in acute coronary syndromes. However, it remains unclear whether BNP directly contributes to cardiovascular disease pathogenesis, such as by promoting thrombosis, or is merely a biomarker. Methods-We assessed the effect of BNP on platelets in vitro and thrombosis in vivo. Platelets were incubated with BNP to measure intracellular cyclic guanosine monophosphate (cGMP) levels and platelet activation markers. BNP was injected into wild-type and NPRA-deficient mice to evaluate its effect on thrombus formation in a FeCl₃ carotid injury-induced arterial thrombosis model and a thromboplastin-induced pulmonary embolism model. BNP receptor natriuretic peptide receptor-A (NPRA) expression in platelets was determined by RT-PCR and Western blot. Results-BNP significantly elevated platelet cGMP and potentiated platelet aggregation, granule secretion, spreading, and clot retraction in vitro. In vivo, BNP administration accelerated thrombus formation in both arterial and pulmonary models in wild-type mice. These prothrombotic effects were abrogated in NPRA-deficient mice. NPRA-deficient mice exhibited impaired platelet activation, prolonged tail bleeding times, and longer occlusion times in the arterial injury model. BNP injection failed to promote thrombosis in NPRA-deficient mice. Conclusions-Our study demonstrates that BNP promotes platelet activation and enhances arterial thrombosis and thromboembolism via NPRA signaling. These findings suggest that BNP is not only a biomarker of cardiovascular disease, but also active effector contributing to thrombosis in cardiovascular disease.

  PublisherOA PDFDOI

• Design and Pharmacological Characterization of a Novel Antithrombotic P2Y1 Receptor-Based Vaccine

  International Journal of Molecular Sciences · 2025-05-05 · 1 citations

  articleOpen accessSenior authorCorresponding

  Platelet activation processes begin when injury to blood vessels exposes the subendothelial matrix, leading platelets to attach to it, where they become activated and exert their hemostatic function. Excessive platelet aggregation is associated with thrombotic disorders such as arterial thrombosis. To manage such diseases, medications that inhibit thrombosis are continuously sought, despite potential drawbacks that include hemorrhage. This study described the development of a novel peptide-based vaccine that targets the purinergic ADP P2Y1 receptor (abbreviated EL2Vac) and its pharmacological characterization. Thus, we designed and developed an EL2Vac that targets the ligand-binding domain of the P2Y1 receptor protein, which is located in its second extracellular loop (EL2). We then evaluated the vaccine’s ability to trigger an immune response (antibody production) in immunized mice, modulate platelet function, its antithrombotic activity, and any effects on hemostasis, by employing a thrombosis model and the tail bleeding time assay. Results showed significant levels of antibody production in mice treated with EL2Vac, in comparison with the random peptide vaccine control (EL2rVac), which persisted at least up to six months post vaccination. Moreover, we observed significant inhibition of the ADP-induced aggregation response in platelets from EL2Vac-treated mice, relative to those from EL2rVac controls. This inhibition was selective for ADP, as other agonists, such as the thromboxane A2 receptor (TPR) agonist U46619 or high-dose collagen, had no detectable effect on aggregation. As for its capacity to protect against thrombosis, our data showed a significant delay in the occlusion time of the EL2Vac mice when compared with the random peptide control vaccine, which was also observed (at least) six months post vaccination. Interestingly, EL2Vac did not appear to prolong the tail bleeding time, supporting the notion that it is devoid of a bleeding diathesis. As a conclusion, this study documents the design and evaluation of a novel peptide-based vaccine, EL2Vac, which appears to selectively target the P2Y1 receptor and protect against thrombus formation without impairing hemostasis. Thus, EL2Vac may provide a promising clinical option to treat thromboembolic disorders.

  PublisherOA PDFDOI

• Clot formation: Novel regulators, drugs, and targets

  Journal of Pharmacology and Experimental Therapeutics · 2025-10-01

  editorialSenior author
  PublisherDOI

• Selective Vaccination-Based Approach Targeting the Platelet Serotonin 5-HT2AR: Potential for Managing Thrombus Formation (Abstract ID: 165403)

  Journal of Pharmacology and Experimental Therapeutics · 2025-03-01

  article
  PublisherDOI

• Impact of smoking on the complement system: a narrative review

  Frontiers in Immunology · 2025-06-19 · 3 citations

  reviewOpen accessSenior authorCorresponding

  Smoking is a major cause of morbidity and mortality, resulting in an increased risk of cardiovascular, respiratory, inflammatory, and degenerative diseases. In this review, we highlight the complex interactions between smoking and activation of different components of the complement system, in order to underscore the notion that its dysregulation underlies-mechanistically-as well as exacerbates the progression of a host of disease processes. Moreover, we also briefly delve into components of tobacco smoke-including chemical constituents like tobacco glycoprotein (TGP) and particulate matter (PM), toxic metals, and other mainstream cigarette smoke chemicals-that have been identified as possible culprits in complement activation. In doing so, this review makes important and meaningful contributions to the ongoing efforts of combating the global health crisis posed by tobacco use, all while emphasizing the need for multifaceted strategies that include not only public health measures and educational efforts, but also innovative research that focuses on understanding and mitigating the biological mechanisms underlying smoking-related health conditions.

  PublisherOA PDFDOI

• Managing thrombus formation with EL2-5HTVac: A selective vaccination-based approach targeting the platelet serotonin 5-HT2AR

  Journal of Pharmacology and Experimental Therapeutics · 2025-02-11 · 5 citations

  article
  PublisherDOI

Recent grants

• The Effects of Prenatal Thirdhand E-cigarette Exposure on Platelets

  NIH · $483k · 2022–2026

• In Utero Third-Hand Smoke Impact on Platelet Function and Thrombogenesis

  NIH · $416k · 2020–2022

• The Mechanistic Impact of Paternal Electronic Nicotine Delivery Systems Exposure on Thrombogenesis

  NIH · $2.9M · 2019–2029

• NIH Grant R15HL115567

  NIH · $838k · 2016

Frequent coauthors

• Fatima Z. Alshbool

  Texas A&M University – Kingsville

  69 shared

• Ahmed B. Alarabi

  Pharmaceutical Biotechnology (Czechia)

  53 shared

• Zubair A. Karim

  Augusta University Health

  38 shared

• Kenji Mizuguchi

  Protein Research Foundation

  28 shared

• Harold J. Ting

  University of Montana

  19 shared

• Enma Verónica Paez Espinosa

  Pontificia Universidad Católica del Ecuador

  19 shared

• John P. Murad

  City of Hope

  14 shared

• Attayeb Mohsen

  National Institute of Biomedical Innovation, Health and Nutrition

  14 shared

Labs

• Pharmaceutical SciencesPI

Awards & honors

• Presidential Impact Fellow