About

Professor Mahua Choudhury 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, background, or key contributions. The content primarily discusses the college's initiatives for first-generation students and features personal stories of students and faculty, including a narrative from Indra K. Reddy, PhD, FAAPS, FAPhA, who is the Founding Dean of the college. There is no explicit biographical or research information about Professor Mahua Choudhury in the provided text.

Research topics

• Medicine
• Biology
• Internal medicine
• Endocrinology
• Cancer research
• Immunology
• Environmental health
• Pathology

Selected publications

• Abstract 4372703: Sex-specific differences in the mechano-metabolic behavior of the myocardium in mice

  Circulation · 2025-11-03

  article

  Introduction: The pathophysiological mechanisms of left ventricular diastolic dysfunction (LVDD) involve impaired relaxation and restricted filling of the left ventricle (LV). Both mechanical and metabolic impairments are expected to occur in the myocardium in LVDD. The mechano-metabolic interplay underlying LVDD-related remodeling remains understudied. Understanding this interplay is especially important for identifying sex-specific susceptibilities to LVDD. In this study, we present an approach to assess key biomechanical and energetic differences through ex-vivo benchtop assays of cardiac mechanoenergetics. Methods: M ale (n=8) and f emale (n=8) 8-10-week-old wild-type mice were used. The LV free wall (LVFW) was harvested from the mice and immediately placed in PBS at 1°C. Mechanical testing was performed to measure passive stiffness and viscoelastic relaxation time (M and F; n = 4 each). The ex-vivo tissue was subjected to equibiaxial stretch at 1% per second and allowed to relax for a period of 10 minutes. Energetics were quantified by homogenizing 10 mg of LVFW tissue using buffer A and analyzing the supernatant ATP concentration (M and F; n = 4 each). Results: Sex differences were evident in both passive mechanical and metabolic indices of LVFW tissues. Stress-strain analysis revealed significantly higher total stress in male mice compared to females at various stages of equibiaxial stretching (Fig. 1A). However, a very similar viscoelastic relaxation behavior was observed between male and female (Fig. 1B). Despite the presence of increased LVFW stiffness in the male mice (Fig. 1C), consistent relaxation time constants were maintained between all mice, evidenced via similar standard deviation (Fig. 1D). Energetic analysis showed a significant difference between male and female mice (M vs. F: 1.75 ± 0.58 vs. 0.48 ± 0.15 nmol) (Fig. 1E). Conclusion: This study provided ex vivo insights into sex-specific mechano-metabolic markers of the myocardial tissue in mice. Our findings demonstrate that male mice possess stiffer myocardial tissue and higher basal ATP concentrations compared to females, despite similar stress relaxation kinetics. Future work using this approach will investigate the mechano-metabolic remodeling in LVDD that accounts for sex-based physiological differences in myocardial stiffening and metabolic impairments.

  PublisherDOI

• Micro- and nanoplastics: Emerging environmental threats to the Developmental Origins of Health and Disease

  Reproductive Toxicology · 2025-11-04 · 3 citations

  articleOpen accessSenior authorCorresponding

  Environmental exposure to micro- and nanoplastics (MNPs) can have significant impacts on the development of chronic health conditions in children and adults. MNPs are byproducts generated from the ubiquitous and daily use of plastics. A growing body of literature points to MNPs’ affecting human metabolic and reproductive health, yet research into their potential impacts is still in its infancy. Due to recent evidence demonstrating accumulation of MNPs within human metabolic and reproductive tissues, their potential for inducing physiological and epigenetic dysregulations is postulated. This is especially critical for future generations as epigenetic disturbances within individuals can be inherited. Currently, the mechanisms for how MNPs exert their effects are still under investigation. In this scenario, the developmental origins of health and disease (DOHaD) offers insight on the influence of environmental exposures in the periconceptual, fetal, and early phases of life towards the development of noncommunicable diseases later in life. DOHaD investigates these interactions through an epigenetic lens as epigenetics bridges environmental exposures and changes in gene expression outside of the DNA sequence itself. In this review, we provide an overview on current research that describes MNPs’ contribution towards the development of metabolic and reproductive dysfunction as well as their potential to impact future generations through the DOHaD paradigm possibly mediated by epigenetic modifications. • MNPs are highly present in the environment due to frequent, wide-spread plastic use • MNP exposure routes include inhalation, ingestion, injection, and dermal absorption • MNPs accumulate in human tissues to possibly impact metabolic & reproductive health • MNPs may exert their toxicities via potentially altering epigenetic modifications • In line with DOHaD, MNPs may affect future offspring by impacting parental health

  PublisherDOI

• Exploring the mechanisms of epithelial-mesenchymal transition (EMT) in breast cancer: The role of MicroRNA and the therapeutic promise of bioactive compounds from edible plants

  Journal of Molecular Structure · 2025-07-02 · 2 citations

  article
  PublisherDOI

• Corrigendum to “Obesity II: Establishing causal links between chemical exposures and obesity” [Biochem. Pharmacol. 199 (2022) 115015]

  UNC Libraries · 2025-04-17

  erratumOpen access
  PublisherDOI

• Early-Life Exposure to Organic Chemical Pollutants as Assessed in Primary Teeth and Cardiometabolic Risk in Mexican American Children: A Pilot Study

  International Journal of Environmental Research and Public Health · 2025-09-27

  articleOpen access

  Early-life exposure to organic chemicals (OCs) may influence childhood obesity and associated cardiometabolic risk. These conditions have been shown to disproportionately affect minority populations such as Mexican Americans (MAs). However, information on the impact of organic chemicals on cardiometabolic risk in MA children is limited. Therefore, we conducted a pilot study to assess the extent to which exposure to organic chemicals influences cardiometabolic traits (CMTs) in MA children. We recalled 25 children from a previous study and collected 25 primary teeth from them. Chemical analyses of the teeth were performed using established protocols. Target analytes included acetaminophen (APAP); 3,5,6-trichloro-2-pyridinol (TCPy), 2-isopropyl-6-methyl-4-pyrimidinol (IMPy), diethyl phosphate (DEP), N,N-diethyl-m-toluamide (DEET), tris(2-butoxyethyl) phosphate (TBOEP), monoethyl phthalate (MEP), mono-n-butyl phthalate (MnBP), monoisobutyl phthalate (MiBP), monobenzyl phthalate (MBzP), mono-2-ethylhexyl phthalate (MEHP), mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP). The organic chemicals most frequently detected in the teeth were APAP; the insect repellent DEET; plasticizers MnBP and MiBP; and the plasticizer-derived metabolite MEHP. These five analytes were included in association analyses with selected CMTs. After adjusting for covariate (age, sex, tooth-type) effects, we found significant (p < 0.05) positive correlations between MiBP and the following CMTs: fat mass, fasting insulin, and the homeostasis model of assessment-insulin resistance (HOMA-IR). Both MnBP and MEHP exhibited negative correlation with blood pressure measures and triglycerides, respectively. In addition, APAP showed a strong negative correlation with HDL-C (p = 0.009) and positive association with triglycerides (p < 0.10). These findings suggest a potential role for early-life exposures to organic chemicals in influencing cardiometabolic risk in MA children.

  PublisherOA PDFDOI

• Environmental Toxicants in the Hispanic Community Epigenetically Contributing to Preeclampsia

  Cardiovascular Toxicology · 2025-07-31 · 1 citations

  reviewOpen accessSenior author

  Preeclampsia is a multisystemic cardiovascular pregnancy complication that endangers the lives of both mother and child. Its prevalence disproportionately burdens women of different races and ethnicities nationwide. Specifically, Hispanic women experience higher rates of preeclampsia compared to Non-Hispanic White women; however, the explanation for this phenomenon is still elusive. To decipher these disparate rates, environmental factors that the Hispanic community is excessively exposed to may need to be considered. Environmental toxicants such as particulate matter, heavy metals, phthalates, as well as microplastics and nanoplastics are ubiquitous within the Hispanic environment. From places of employment to in the home, the role of chronic toxicant exposure in Hispanic women may begin to explain the gap in the prevalence of preeclampsia development. To understand the relationship between toxicant exposure and preeclampsia, we explored epigenetic concepts. With the capacity to respond to the environment in a heritable and reversible manner, epigenetics changes the expression of genes and proteins while leaving the DNA sequence intact. Epigenetic modifications can be dysregulated upon toxicant exposure and can potentially lead to the development of preeclampsia. Here, in this review, we propose the potential epigenetic links through which Hispanic women's disproportionate environmental exposure to toxicants can be conducive to preeclampsia development.

  PublisherOA PDFDOI

• Phthalates and epigenetics: An emerging public health concern

  Current Research in Toxicology · 2025-01-01 · 5 citations

  articleOpen access

  • Phthalate exposure induces organ-specific epigenetic alterations , including in genes regulating hormone signaling and development. • We synthesize evidence for transgenerational inheritance of phthalate-induced epigenetic marks in animal models. • Key mechanisms are detailed, such as the disruption of DNMT and HAT activity and the role of androgen receptor signaling . • Epigenetic changes are critically linked to ADHD, infertility, metabolic syndrome, and testicular dysgenesis . • We discuss the potential and significant limitations of epigenetic therapies in counteracting phthalate toxicity. Phthalates are a group of phthalic acid esters that are commonly used as plasticizers in many consumer products to improve elasticity, transparency, durability, and toughness. Phthalates are also ubiquitously found throughout our environment. In recent years, research has indicated a growing concern over the potential negative health effects that phthalates have on the human body. Considering their presence in a wide range of consumer goods, including food packaging, household goods, medical equipment, and personal hygiene products, humans are continuously exposed to many phthalates in their everyday lives. More strikingly, exposure to phthalates has been shown to induce abnormal epigenetic changes in noncoding RNA expression, DNA methylation, and histone modification. Epigenetic changes are critical in governing gene expression while leaving the DNA sequence intact. Previous studies have established the role of aberrant epigenetic changes in the pathogenesis of many diseases, including cancer and endocrine diseases related to phthalate exposure. The purpose of this review is to provide insight into the mechanisms by which phthalates may affect epigenetic processes and the potential adverse health consequences of these interactions.

  PublisherDOI

• A dual-modality paper fluidic platform to detect an extended range of microRNA-20a related to preeclampsia

  Microchemical Journal · 2025-09-10

  article
  PublisherDOI

• Potential Regulatory Role of miR-15b, miR-99b, and miR-181a of the Shikonin-Induced MAPK/ERK Apoptotic Signaling Pathway in Renal Carcinoma

  Biomedicines · 2025-11-27

  articleOpen access

  Background: Shikonin, a natural compound derived from Lithospermum erythrorhizon, exhibits anticancer properties by inducing apoptosis in various tumor types, including clear cell renal cell carcinoma (ccRCC) cell lines CAKI-2 and A-498. This study investigates the mechanisms underlying shikonin-induced apoptosis, focusing on microRNAs miR-15b, miR-99b, and miR-181a in ccRCC. Materials and Methods: ccRCC cells were treated with 5 µM shikonin. Expression levels of miR-15b, miR-99b, and miR-181a were measured by TaqMan PCR. Apoptosis-related targets (AKT3, PDCD4, FOXO1, FOXO3, JNK1, and LAMTOR3) were identified in silico and validated by qRT-PCR and Western blot. Spearman’s correlation was used to evaluate miRNA–target relationships. Ingenuity Pathway Analysis explored relevant pathways. Results: Shikonin decreased miR-15b, miR-99b, and miR-181a levels in CAKI-2 cells, whereas these miRNAs were increased in A-498 cells, demonstrating cell-line-specific effects. qRT-PCR and Western blot confirmed changes in target expression, suggesting regulation by these miRNAs. In A-498 cells, miR-181a expression positively correlated with the studied target levels during 24–72 h of treatment, indicating that its potential regulatory role may be cell-type-dependent. MiR-15b and miR-99b showed linear correlations with targets in both cell lines, but expression patterns differed, suggesting direct regulation alongside potential involvement in additional pathways contributing to shikonin-induced apoptosis. Conclusions: Shikonin induces apoptosis in renal cancer cells by modulating the MAPK/ERK pathway and through cell-line-specific, cell-type-dependent regulation of miR-15b, miR-99b, and miR-181a. These findings highlight the importance of cell-type-dependent miRNA regulation and underscore the therapeutic potential of shikonin in ccRCC.

  PublisherOA PDFDOI

• Abstract Fri023: Integrated mechano-metabolic measures of diastolic function in mice

  Circulation Research · 2025-08-01

  article

  Introduction: Impaired left ventricular (LV) relaxation, a consequence of left ventricular diastolic dysfunction (LVDD), is a common sequela of cardiometabolic diseases. While separate endeavors have been devoted to studying the mechanical and metabolic mechanisms of diastolic function, the physiological link across mechano-metabolic cues governing relaxation remains understudied. Herein, we present a platform for measuring mechano-metabolic indices of diastolic function in mice through in-vivo echocardiography, followed by ex-vivo benchtop testing of mechanics and energetics. Methods: Male, 8-10-week-old wild-type mice were used. Early transmitral flow to mitral annular tissue velocity ratio (E/e’), measured by Doppler imaging, was used to assess LV relaxation. The LV free wall (LVFW) was harvested from the mice and immediately placed in PBS at 1°C. Mechanical testing was performed to measure stiffness (n = 4). Additionally, energetics were quantified by homogenizing 10 mg of LVFW tissue using buffer A and analyzing the supernatant ATP concentration (n = 4). Results: A bias in passive stresses towards the circumferential direction, in comparison to the longitudinal direction, was noted at various stages of equibiaxial stretching (Fig. 1A). A similar anisotropic behavior was confirmed via LVFW stiffness (Fig. 1B). A consistent spread in E and e’ was maintained in all mice, evidenced via similar standard deviation (Fig. 1C). Baseline diastolic function was established using the E/e’ ratio (Fig. 1D), and the average basal ATP levels in mice was measured as 1.75 ± 0.58 nmol (Fig. 1E). Conclusion: The integration between in-vivo echocardiography and ex-vivo mechanical testing and metabolic assays was established in mice. This platform will enable us to determine the relationship between mechanical and metabolic alterations in LVDD, thereby optimizing patient-specific therapies based on these integrated measures of diastolic function.

  PublisherDOI

Frequent coauthors

• Sunitha Meruvu

  Texas A&M Health Science Center

  17 shared

• Gerard L. Coté

  Texas A&M Engineering Experiment Station

  15 shared

• Catherine A. Powell

  12 shared

• Shaikh Mizanoor Rahman

  11 shared

• Matthew Kay

  Yancheng Teachers University

  11 shared

• Monika Schechinger

  Texas A&M University

  9 shared

• Shivendra D. Shukla

  9 shared

• Min Hi Park

  Kyungsung University

  9 shared

Labs

• Pharmaceutical SciencesPI

Awards & honors

• Presidential Impact Fellow