About

Daniela Valdez-Jasso is an Associate Professor of Bioengineering and a Faculty-Affiliate of Mechanical and Aerospace Engineering at the University of California, San Diego. Her research focuses on soft-tissue biomechanics and multi-scale mathematical modeling of organ and tissue function, with particular emphasis on understanding the ventriculo-vascular adaptations to pulmonary hypertension (PH). Her group aims to understand the dynamic vascular remodeling process in PH at the tissue level and its effects at the system level, integrating experimental findings into mechanistic mathematical models for quantitative analysis of organ and tissue function. Valdez-Jasso received her undergraduate and master's degrees in Applied Mathematics, and her doctoral degree in Biomathematics from North Carolina State University. Her graduate thesis, recognized with a Lucas Research Award, involved modeling the pressure-area relationship of systemic arteries. During her postdoctoral training at the University of Pittsburgh School of Medicine, she investigated the tissue structure and biomechanics of the normal and pressure-overloaded right ventricle, supported by an American Heart Association postdoctoral fellowship. She has established her research laboratory at the University of Illinois at Chicago, focusing on soft-tissue biomechanics and multi-scale modeling related to vascular and right-ventricular adaptations to pulmonary hypertension. Her work is currently supported by an American Heart Association Scientist Development Grant. Valdez-Jasso has also been active in mentoring and diversity initiatives, including the Minority Engineering Recruitment and Retention Program at UIC and serving as vice-chair of the Diversity and Inclusion Committee of the American Society of Mechanical Engineering Bioengineering Division.

Selected publications

• Sex and Ovarian Hormone Status Shape Baseline Cardiovascular Physiology in Sprague–Dawley Rats

  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · 2026-05-14

  articleSenior author

  Sex is increasingly recognized as a critical biological variable in preclinical cardiovascular research yet baseline physiological differences between male and female animals-and the experimental decisions that shape their interpretation-remain incompletely defined. Here, we establish a quantitative experimental framework by systematically characterizing growth trajectories, cardiac scaling, anesthetic sensitivity, estrous-cycle effects, and myocardial mechanics in male, ovary-intact female, and ovariectomized (OVX) female Sprague-Dawley rats. Marked sex- and hormone-dependent differences in body growth rendered simultaneous age- and weight-matching impractical and led to distinct - and sometimes opposing - inferences regarding normalized cardiac mass depending on cohort standardization strategy. Baseline hemodynamics were comparable across sex and estrous stage, whereas ovarian hormone status modulated right ventricular structure and passive myocardial mechanics. Physiological fluctuations in estrogen were associated with estrogen-dependent changes in right ventricular mass, thickness, and compliance, while early ovariectomy produced persistent increases in myocardial stiffness independent of hemodynamic load. OVX females also exhibited heightened sensitivity to isoflurane during surgical procedures, particularly during early operative phases. Together, these findings demonstrate that sex, circulating estrogen, and timing of ovarian hormone loss shape baseline cardiovascular phenotypes. Rather than treating sex-related variability as experimental noise, this study provides practical guidance for experimental design, normalization, and interpretation in preclinical cardiovascular research.

  PublisherDOI

• Mechanical Remodeling of the Left and Right Pulmonary Arteries in Sugen-Hypoxia Rat Model of Pulmonary Arterial Hypertension

  SSRN Electronic Journal · 2026-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Pulmonary Arterial Hypertension Induces Sex-Specific Right Ventricular Transcriptomic Remodeling

  Physiology · 2026-05-01

  articleSenior author

  Objective: Pulmonary arterial hypertension (PAH) imposes chronic pressure overload on the right ventricle (RV), leading to progressive remodeling and ultimately RV failure, the primary cause of mortality in the disease. Although PAH is more prevalent in women, men exhibit worse RV outcomes, underscoring the importance of sex-specific mechanisms governing RV adaptation and failure. Importantly, ventricular diastolic stiffening is a strong predictor of disease severity and poor prognosis, and prior hemodynamic and tissue-level studies indicate that RV remodeling transitions from compensatory hypertrophy to maladaptive stiffening as disease progresses. Here, we investigate whether sex-dependent RV transcriptomic remodeling reflects distinct trajectories toward ventricular stiffening and dysfunction. Methods: PH was induced in male and female Sprague-Dawley rats using the sugen-hypoxia (SuHx) model. Bulk RNA sequencing was performed on RV tissue after 4 and 8 weeks of SuHx, with confirmed hypertension and tightly distributed end-systolic and end-diastolic pressures. Equal-sized normotensive groups served as controls. Data were processed in Galaxy through differential expression analysis, with downstream processing and visualization performed using R and Gene Set Enrichment Analysis (GSEA). Results: RV transcriptomes clustered primarily by sex and treatment, without distinguishing SuHx timepoints, indicating early establishment of disease-specific transcriptional programs (Figure 1). SuHx induced enrichment of profibrotic, inflammatory, and apoptotic pathways, while suppressing key metabolic pathways (Figure 2). At baseline, male RVs exhibited higher enrichment of profibrotic and inflammatory pathways and reduced metabolic signaling compared with females, suggesting a predisposition toward stress-sensitive remodeling. After accounting for these baseline differences, female SuHx RVs showed greater enrichment of proliferation and angiogenic pathways (Figure 2). In contrast, male SuHx RVs reached greater absolute enrichment of profibrotic and apoptotic pathways, accompanied by pronounced suppression of mitochondrial metabolism. Notably, these transcriptional signatures correspond to higher end-systolic and end-diastolic pressures in male animals relative to stage-matched females, reflecting greater mechanical disease severity. Conclusions: These findings suggest that male RV exhibit a transcriptional profile characterized by heightened stress signaling, metabolic dysfunction, and cell death, which are features consistent with accelerated ventricular stiffening and progression toward failure. In contrast, female RVs engage transcriptional programs favoring extracellular matrix remodeling and cellular proliferation, indicating a more adaptive response to pressure overload. Together, these results link sex-dependent transcriptomic remodeling to organ-level hemodynamic severity and support ventricular stiffening, rather than hypertrophy alone, as a key determinant of maladaptive RV remodeling and outcomes in PAH. Funding: NSF CAREER 2046259, NHLBI 1R01HL155945, Conrad Prebys Foundation This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

  PublisherDOI

• Adventitial Fibrosis and Fibroblast Mechanosensitivity Are Shaped by Sex and Hormonal Status in Pulmonary Arterial Hypertension

  Cells · 2026-02-16

  articleOpen accessSenior authorCorresponding

  Pulmonary arterial hypertension (PAH) is marked by vascular remodeling, yet the role of adventitial fibrosis-and its modulation by sex and hormonal status-remains unclear. We examined stage-specific adventitial remodeling and pulmonary artery adventitial fibroblast (PAAF) mechanosensitivity in male, ovary-intact female, and ovariectomized (OVX) female Sprague-Dawley rats with SuHx-induced PAH. Hemodynamics, pulmonary artery histology, and adventitia-specific transcriptional profiling were integrated with in vitro assays of PAAFs exposed to defined substrate stiffness and stretch. All groups developed comparable increases in mean pulmonary arterial pressure, but vascular resistance shift and adventitial fibrosis diverged by sex: intact females showed attenuated increase in pulmonary vascular resistance and transient collagen accumulation, whereas OVX females mirrored the sustained, male-like progression. Extracellular matrix (ECM) gene activation occurred without smooth muscle actin induction, suggesting noncanonical fibrotic pathways. In vitro, intact female PAAFs required higher substrate stiffness to induce profibrotic gene expression, indicating a hormone-modulated stiffness threshold. OVX PAAFs showed persistent transcriptional reprogramming, while stretch-induced ECM upregulation occurred predominantly in male-derived PAAFs. These findings demonstrate that adventitial fibrosis in PAH is shaped by both hormonal and chromosomal sex, independent of hemodynamic severity, and highlight fibroblast mechanosensitivity as a potential target for stage- and sex-specific interventions.

  PublisherOA PDFDOI

• Feasibility of 4D flow hemodynamics as an indicator of RV dysfunction in patients with transposition of the great arteries

  Journal of Cardiovascular Magnetic Resonance · 2025-01-01

  articleOpen access
  PublisherDOI

• Sex-Specific Interventricular Septum Mechanics in Pulmonary Arterial Hypertension

  Annals of Biomedical Engineering · 2025-11-04

  articleSenior author
  PublisherDOI

• Ovarian hormones attenuate right ventricular remodeling in a rat model of pulmonary arterial hypertension

  Biomechanics and Modeling in Mechanobiology · 2025-12-17

  articleSenior author
  PublisherDOI

• A computational study of right ventricular mechanics in a rat model of pulmonary arterial hypertension

  Frontiers in Physiology · 2024-03-11 · 5 citations

  articleOpen access

  Pulmonary arterial hypertension (PAH) presents a significant challenge to right ventricular (RV) function due to progressive pressure overload, necessitating adaptive remodeling in the form of increased wall thickness, enhanced myocardial contractility and stiffness to maintain cardiac performance. However, the impact of these remodeling mechanisms on RV mechanics in not clearly understood. In addition, there is a lack of quantitative understanding of how each mechanism individually influences RV mechanics. Utilizing experimental data from a rat model of PAH at three distinct time points, we developed biventricular finite element models to investigate how RV stress and strain evolved with PAH progression. The finite element models were fitted to hemodynamic and morphological data to represent different disease stages and used to analyze the impact of RV remodeling as well as the altered RV pressure. Furthermore, we performed a number of theoretical simulation studies with different combinations of morphological and physiological remodeling, to assess and quantify their individual impact on overall RV load and function. Our findings revealed a substantial 4-fold increase in RV stiffness and a transient 2-fold rise in contractility, which returned to baseline by week 12. These changes in RV material properties in addition to the 2-fold increase in wall thickness significantly mitigated the increase in wall stress and strain caused by the progressive increase in RV afterload. Despite the PAH-induced cases showing increased wall stress and strain at end-diastole and end-systole compared to the control, our simulations suggest that without the observed remodeling mechanisms, the increase in stress and strain would have been much more pronounced. Our model analysis also indicated that while changes in the RV's material properties-particularly increased RV stiffness - have a notable effect on its mechanics, the primary compensatory factor limiting the stress and strain increase in the early stages of PAH was the significant increase in wall thickness. These findings underscore the importance of RV remodeling in managing the mechanical burden on the right ventricle due to pressure overload.

  PublisherOA PDFDOI

• Sex-dependent remodeling of right ventricular function in a rat model of pulmonary arterial hypertension

  American Journal of Physiology-Heart and Circulatory Physiology · 2024-06-07 · 11 citations

  articleOpen accessSenior author

  Combining hemodynamic and morphological measurements from male, female, and ovariectomized female pulmonary arterial hypertension (PAH) rats revealed distinct adaptation mechanisms despite similar pressure overload. Males showed the most diastolic stiffening. Ovariectomized females had enhanced myocyte contractility and calcium transient upregulation. Ovary-intact females primarily responded with hypertrophy, experiencing milder passive myocardial stiffening and no changes in myocyte shortening. These findings suggest potential sex-specific pathways in right ventricular (RV) adaptation to PAH, with implications for targeted interventions.

  PublisherOA PDFDOI

• Editorial: Computational models of cardiovascular growth and remodeling

  Frontiers in Physiology · 2023-01-23 · 2 citations

  editorialOpen accessSenior author

  For the last couple of decades, a growing trend in computational cardiovascular research has been to 50 move away from generalized and simplistic models to personalized and patient-specific models. In spite of 51 substantial research effort and a continuous push for models representing precision medicine, however, 52 seemingly obvious differences such as those between male and female hearts remain understudied and 53 often neglected. The paper from St. Pierre et al presents a systematic review of the anatomy, function, 54 and physiological adaptation found in male and female hearts. The study reveals a range of significant 55 differences, and argue for increased research and design of sex-specific diagnostic criteria for earlier and 56 more precise diagnosis of cardiac disease in women. provide support for previous experimental results on the impact of pericardiectomy on cardiac function.The final contribution in this special issue, from Odeigah et al is also focused on pulmonary hypertension

  PublisherOA PDFDOI

Awards & honors

• Lucas Research Award