About

Professor Fatima Alshbool is associated with the Texas A&M Irma Lerma Rangel College of Pharmacy. The provided page text does not include specific details about her research focus, academic background, or key contributions. The content primarily discusses the college's initiatives for first-generation students and shares personal stories of first-generation students, including a narrative from Indra K. Reddy, PhD, and Cassandra Lee Cruz, but does not mention Professor Alshbool's professional biography or research activities.

Research topics

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

Selected publications

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

  Experimental Biology and Medicine · 2026-03-12

  articleOpen access

  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 accessSenior author

  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

• 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

  articleSenior author
  PublisherDOI

• 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 accessSenior author

  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

• Alterations in the Platelet Transcriptome Mediate Prenatal Thirdhand Smoke Exposure Associated Thrombogenicity via Integrated miRNA-mRNA Regulatory Networks

  International Journal of Molecular Sciences · 2025-08-07 · 2 citations

  articleOpen access

  Cigarette smoking is acknowledged as the most preventable risk factor for thrombogenesis-associated cardiovascular disease. Mice prenatally exposed to the thirdhand smoke (THS) form of tobacco exhibited a higher tendency to develop occlusive thrombosis, along with enhancement of several platelet functional responses. Our objective was to investigate whether prenatal (in utero) THS exposure impacts the platelet transcriptome, resulting in enhanced platelet functional responses, thereby underlying THS-associated thrombogenicity. Blood samples obtained from twenty male mice prenatally exposed to THS, along with an equal number of age-matched male mice exposed to clean air (CA) as a control, were divided into pools of five animals and used to prepare leukocyte and red blood cell-depleted platelets. RNA sequencing for mRNA and microRNA (miRNA) was utilized to analyze and compare the platelet expression profiles of the two exposure groups. RNA seq analyses revealed distinct changes in both gene expression and miRNA profiles, with 448 coding genes and 18 miRNAs significantly altered between the two groups. miRNA-mRNA interaction analysis highlighted 14 differentially expressed miRNAs that potentially target 120 of the differentially expressed genes in our data set. Interestingly, altered genes in miRNA-mRNA pairs were functionally enriched into pathways associated with platelet physiology, including platelet activation, signaling and aggregation, and cellular response to chemical stimuli. Our findings establish-for the first time-that prenatal exposure to THS modifies the platelet transcriptome, thereby rendering platelets hypersensitive to stimuli and more prone to thrombogenicity. Additionally, we illuminate the coordinated function of platelet miRNA and mRNA targets in mediating this response.

  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 access

  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

• The Impact of Maternal/In Utero Exposure of Novel Tobacco Products on the Offspring Cardiovascular Health

  Cardiovascular Toxicology · 2025-06-20

  reviewOpen accessSenior authorCorresponding

  Novel tobacco products (NTPs) have recently been on the rise appealing to a variety of users, including pregnant women and women of childbearing age, who deem these products to be a safe/safer alternative to traditional smoking. To this end, several studies have made advances toward proving the invalidity of these claims, especially in the context of cardiovascular disease. However, an area that has yet to be extensively explored is maternal/in utero exposure to these devices and the cardiovascular health outcomes on the offspring into their adult life. Herein, our aim is to critically assess the literature to identify and discuss the cardiovascular health risks that the offspring exhibits as a result of in utero exposure to NTPs. These studies have been summarized as a comprehensive review.

  PublisherOA PDFDOI

• 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

  articleSenior author
  PublisherDOI

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

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

  reviewOpen access

  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

• Investigation of the impact of thirdhand e-cigarette exposureon platelet function: A pre-clinical study

  Tobacco Induced Diseases · 2024-03-30 · 6 citations

  articleOpen accessSenior authorCorresponding

  INTRODUCTION: The use of e-cigarettes (ECs) has reached unprecedented levels, due to a variety of reasons, including the misconception regarding their safety. Thus, there have been efforts to characterize the effects of EC exposure, including in the context of thirdhand EC (THEC) on a host of disorders, such as cardiovascular disease (CVD). METHODS: platelet specific (e.g. aggregation, and dense granule secretion) investigative assays were conducted. RESULTS: characterization demonstrated that THEC exposed mice exhibited a prothrombotic phenotype reflected by their shortened tail bleeding (THEC: 37 ± 15 seconds, versus clean air: 183 ± 56 s) and occlusion times (THEC: 188 ± 39 s, versus clean air: 519 ± 70 s), relative to those exposed to clean air. Importantly, we found no difference in the platelet counts between the THEC and clean air mice. As for the underlying mechanism, separate experiments revealed significantly enhanced platelet aggregation, dense and alpha granule secretion, as well as integrin/GPIIb-IIIa activation and phosphatidylserine exposure in response to thrombin and ADP agonist stimulation. CONCLUSIONS: Taken together, these results provide evidence that THEC does have the capacity to increase the risk of thrombotic disease, which should increase awareness regarding its underappreciated negative health effects.

  PublisherOA PDFDOI

Recent grants

• Investigate the mechanism and impact of E-cigarettes on platelet function and thrombogenesis

  NIH · $535k · 2022–2024

• The Impact of Third-Hand E#Cigarette Exposure on Platelet Function and Thrombogenesis

  NIH · $152k · 2020–2023

• The Impact of In Utero E-Cigarette Exposure on Platelet Function and Thrombogenesis

  NIH · $417k · 2022–2026

Frequent coauthors

• Fadi T. Khasawneh

  69 shared

• Ahmed B. Alarabi

  Pharmaceutical Biotechnology (Czechia)

  53 shared

• Kenji Mizuguchi

  Protein Research Foundation

  30 shared

• Zubair A. Karim

  Augusta University Health

  26 shared

• Subburaman Mohan

  Loma Linda University

  16 shared

• Attayeb Mohsen

  National Institute of Biomedical Innovation, Health and Nutrition

  15 shared

• Patricia A. Lozano

  11 shared

• Hamdy Ali

  Texas A&M University – Kingsville

  9 shared

Labs

• Pharmaceutical Sciences FacultyPI

Awards & honors

• Presidential Impact Fellow