Search bioRxiv⌕ Search

Biology subjects

Lakshmikanthan, A.

Publications and source records attributed to Lakshmikanthan, A..

2 recordsLinked to original sources

Representing Sex in Cardiovascular Models: Calibrating Reference Parameters from Healthy Cohorts

Reduced-order models are increasingly used to study cardiac physiology and inform patient-specific therapies. However, a model's prediction is only as reliable as its underlying parameters: representative model parameterization is essential to reflect the physiology of the populations these models are meant to represent, including biological sex. Most current models are parameterized from male or sex-agnostic data and/or focus on specific pathologies. Therefore, the goal of this work is to establish a formal parameter estimation pipeline for deriving reduced-order cardiovascular model parameter ranges that are physiologically representative of healthy women and men. We calibrated a closed-loop reduced order model of the heart and circulation separately for healthy female and male populations, using data pooled from eleven healthy cohorts. To account for parameter sensitivity and identifiability, we employed a three-stage parameter subset reduction pipeline: global sensitivity analysis (Sobol's method), collinearity screening (Fisher information matrix), and profile-likelihood identifiability analysis. Sex-specific distributions of parameters that were deemed sensitive and identifiable for each sex, ten for women and 9 for men, were obtained by Hamiltonian Monte Carlo. All the calibrated parameters showed less than 80% overlap between sexes, with the smallest overlap observed in some of the most influential parameters, such as stressed blood volume. Comparing simulations of the calibrated models against allometrically size-matched simulations showed that body size explained some, but not all, of the sex differences. The resulting parameter distributions provide reference ranges usable in future mechanistic and patient-specific simulations to contribute to more inclusive cardiovascular modeling.

bioengineering↗

Modeling the Interplay of Sex Hormones in Cardiac Hypertrophic Signaling

Biological sex plays a crucial role in the outcomes of cardiac health and therapies. Sex hormones are known to strongly influence cardiac remodeling through intracellular signaling pathways, yet their underlying mechanisms remain unclear. To address this need, we developed and validated a logic-based systems biology model of cardiomyocyte hypertrophy that, for the first time, incorporates the effects of both estradiol (E2) and testosterone (T) alongside well-established hypertrophic stimuli (Strain, angiotensin II (AngII), and endothelin-1 (ET-1)). We qualitatively validated the model to literature data with 84% agreement. Quantitative validation was done by simulating the impact of the inputs (E2, T, Strain, AngII, and ET-1) on cardiac hypertrophy, captured as change in CellArea. We perturbed the validated model to examine the differential response to hypertrophy and identify changes in influential and sensitive downstream nodes for a male, pre-menopausal female, and post-menopausal female condition. Our results suggest that T has a greater impact on hypertrophy than E2. This model increases our understanding of the mechanisms through which sex hormones influence cardiac hypertrophy and can aid with developing more effective cardiac therapies for all patients. Author summaryDifferences between female and male hearts extend far beyond size and structure. Sex hormones estradiol and testosterone play key roles in sex-specific cardiac remodeling via intracellular pathways. Understanding how these sex hormones impact cardiac remodeling is critical for developing more effective, sex-specific approaches to cardiovascular care. Logic-based systems biology models have proven useful in quantifying and analyzing complex and intricate intracellular signaling network dynamics in various cell types. We leverage this method to develop a model of cardiomyocyte hypertrophy, which, for the first time, includes the effect of both estradiol and testosterone. Considering the combined influence of these hormones is important because both women and men have varying concentrations of these hormones throughout their lives. The model was developed and validated based on previously published studies. We then investigated differences in cardiomyocyte hypertrophy in pre- and post-menopausal women and men.

systems biology↗