Dr Keqing Wang

Supervisor Details

Contact Details

Scientific Background

Research Interests

Dr Wang is a lecturer in Vascular Inflammation and Associate Dean for Research at Aston Medical School. Dr Wang’s postdoctoral research was funded by European Research Council and Medical Research Council. She has extensive research experience in immunology, inflammation and the vascular biology of pregnancy. Her current research interests focus on the role of gaseous transmitters in the pathogenesis of preeclampsia, fetal growth restriction and cardiomyopathy. She discovered hydrogen sulphide (H2S) as an important regulator of the placental vasculature development and showed that a deficiency in its production causes preeclampsia-like features. This study identified H2S as a potential new target for therapeutic intervention against preeclampsia and fetal growth restriction. This work was highlighted as being a “groundbreaking study” by Circulation and within the media (see: Breakthrough in fight against pre-eclampsiaLink opens in a new window).

Research Themes

Pathogenesis of preeclampsia - research from basic science to preclinical experimental disease models and paves way to development of novel therapies for preeclampsia.
Diagnosis of preeclampsia and fetal growth restriction. Identify novel biomarkers including gaseous molecules, microRNAs and metabolites markers, protein modifications and laser devices.
Development of treatment for preeclampsia and fetal growth restriction.
Vascular homeostasis and chronic inflammation.
Cardiomyopathy in pregnancy.

Supervision Style

In three words or phrases: Supportive: provide good technique training, clear instruction and feedback.

Provision of Training

I prefer to take responsibility for your technical training at first, leading to more independence later.

Your training will be supervised predominantly by myself, associated supervisors and collaborators/PhD students.

Progression Monitoring and Management

I will expect you to take full ownership of your progression but come to me when you need help troubleshooting.

I like to be kept up to date, and will expect to see evidence of method development/data generation results on a weekly basis. I will set out my expectations of your progression on a weekly basis. If these progression criteria are not met we will always discuss a plan of action together.

I have high expectations and will push you to your full potential. I am here for advice and guidance to help you reach the goals you set for yourself.

Communication

I am happy to discuss any issues that are impacting your ability to fulfil your potential or my/our expectations.

PhD Students can expect scheduled meetings with me:

In a group meeting

At least once a week

In year 1 of PhD study

At least once a week

In year 2 of PhD study

At least once a week

In year 3 of PhD study

At least once a week

These meetings will mainly be face to face, and I am usually contactable for an instant response on every working day.

Working Pattern

Certain tasks in my lab need to occur at set times, and students need to be able to commit to a rota/timetable shared with other members of the team.

Notice Period for Feedback

I need at least 2 weeks' notice to provide feedback on written work of up to 5000 words.

MIBTP Project Details

Current Projects (2025-26)

Primary supervisor for:

Investigating the Molecular Mechanisms of Preeclampsia-Induced Cardiovascular Dysfunction Using in vitro Microtissue Models

See the PhD Opportunities section to see if this project is currently open for applications via MIBTP.

Please Note: The main page lists projects via BBSRC Research Theme(s) quoted and then relevant Topic(s).

Investigating the Molecular Mechanisms of Preeclampsia-Induced Cardiovascular Dysfunction Using in vitro Microtissue Models

Secondary Supervisor(s): Dr Shakil Ahmad

University of Registration: Aston University

BBSRC Research Themes:

Understanding the Rules of Life (Systems Biology)
Integrated Understanding of Health (Ageing)

Project Outline

Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide, responsible for an estimated 17.9 million deaths annually. While the incidence of CVD is generally lower in women compared to men, this gender disparity narrows as women age, with elderly women exhibiting a higher prevalence of heart disease. Notably, life events such as pregnancy can substantially increase the risk of CVD at a younger age. As such, CVD is the leading cause of death in new mothers, accounting for over one-third of maternal death. Women with a history of pregnancy complications, such as preeclampsia—a pregnancy-related high blood pressure disorder—are four times more likely to experience future heart failure and myocardial infarction. Additionally, they have a twofold increased risk of early coronary artery disease, stroke, and CVD-related death compared to women with uncomplicated pregnancies. The underlying mechanisms that drive cardiovascular dysfunction during pregnancy and contribute to the increased postpartum cardiovascular risk remain poorly understood.

In our previous studies, we demonstrated that maternal cardiovascular function is compromised during both pregnancy and the postpartum period in a preeclampsia murine model with sFlt-1 overexpression. RNA sequencing revealed significant differences in the gene expression profiles of cardiac tissue during pregnancy and postpartum between sFlt-1 overexpressing preeclamptic mice and control mice, indicating that preeclampsia may have long-term detrimental effects on the cardiovascular system. This project aims to elucidate the common pathological mechanisms underlying preeclampsia-associated cardiovascular dysfunction. These findings could lead to the identification of novel therapeutic targets and the development of new diagnostic and treatment strategies for CVD in women.

Objectives

The overarching goal of this project is to identify molecular targets involved in preeclampsia-induced cardiovascular dysfunction using in vitro models. The specific objectives are:

To use cardiac RNA-sequencing data from an in vivo preeclampsia model, coupled with bioinformatics analysis, to identify molecular signatures and potential interactive pathways.

To generate an in vitro cardiovascular model to assess the short-term and long-term impact of preeclampsia on the cardiovascular system.

To investigate the molecular effects of preeclampsia on the cardiovascular system using various molecular biology techniques.

Methods

Objective 1:
We will analyse cardiac RNA-sequencing data (during pregnancy and postpartum) from an in vivo preeclampsia model to identify molecular signatures and potential interactive pathways. Bioinformatics approaches will be employed to detect differentially expressed genes and pathway enrichment associated with preeclampsia-related cardiovascular dysfunction.

Objective 2:
We will establish 3D human cardiac microtissues composed of commercially available induced pluripotent stem cell-derived cardiomyocytes (iCell2, Cellular Dynamics International) and human umbilical vein endothelial cells (HUVEC). These microtissues will be exposed to sFlt-1 or plasma samples from normal and preeclamptic patients for varying durations (24 hours, 72 hours, 1 week, and 2 weeks) to mimic the short- and long-term effects. Cardiomyocyte morphology, calcium transients, RNA sequencing, quantitative PCR (qPCR), and immunohistochemistry will be used to assess the cellular and molecular effects of preeclampsia.

Objective 3:
RNA-sequencing data from the in vitro cardiovascular model will be compared with data from the in vivo preeclampsia model. Specific molecular targets and interactive pathways will be further investigated using qPCR, Western blotting, immunohistochemistry, and small interfering RNA (siRNA) to dissect the molecular underpinnings of preeclampsia-associated cardiovascular dysfunction.

This project will provide a comprehensive understanding of the molecular mechanisms driving preeclampsia-associated cardiovascular dysfunction and offer insights for developing novel diagnostic and therapeutic interventions.