Zhichao Zhou

Zhichao Zhou

Principal Researcher | Docent
Visiting address: Norrbacka S1:02, Karolinska Universitetssjukhuset Solna, 17176 Stockholm
Postal address: K2 Medicin, Solna, K2 Kardio Pernow J Zhou Z, 171 77 Stockholm
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About me

  • I am an Associate Professor and team leader at Division of Cardiology in the Department of Medicine Solna at Karolinska Institutet. I lead a research team conducting translational research in cardiovascular field with a current focus on diabetes-associated vascular complications. I graduated from a Medical school in China in 2007 and obtained my Ph.D. degree from the Department of Cardiology, Erasmus University Medical Center Rotterdam in the Netherlands in 2013. I had my postdoc trainings at West Virginia University and Karolinska Institutet, respectively (2014-2018). My research focus is on the elucidation of novel disease mechanisms underlying cardiovascular complications and identification of effective therapeutic and diagnostic strategies for patients with cardiometabolic disease suffering from cardiovascular complications.

    My research team has been supported by a number of grants from the following funders:
    * Swedish Research Council (2023)
    * EFSD/Novo Nordisk Foundation Future Leaders Award (2022)
    * Swedish Heart and Lung Foundation (2019, 2020, 2022, 2023 and 2024)
    * Karolinska Institutet KID Funding (2021 and 2023)
    * Eva and Oscar Ahréns Foundation (2021)
    * Loo and Hans Ostermans Foundation (2018 and 2020)
    * Lars Hiertas Minne Foundation (2018)
    * Karolinska Institutet Grant (2018, 2020, 2020 and
    2022 and 2024)
    * Sigurt and Elsa Goljes Memorial Foundation (2017)
    * Olaussons Fund 2016

    Commission of trust:
    * Editorial board: Front Cardiovasc Med; Front Pharmacol; Purinergic Signal; ATVB (early career editorial board)
    * Coordinator of KIRCNET (2020-2023) [1]
    * Committee member: KIRCNET (2023-present), KiiM (2021-2023) [2] and Cardiovascular Research Seminar Series (2022-present)
    * Member of Swedish Cardiometabolic Research Network (SCAMN) (2023-present)
    * The SRP Diabetes PI group (2022-present) [3]
    * Member of EU-CardioRNA COST action (2021-present)
    * Guest editor: Front Cardiovasc Med 2022; Int J Hypertens 2019
    * Grant evaluation task for: UK Medical Research Council (MRC); Polish National Science Center and Health Research Council of New Zealand
    * Journal reviewer for: J Am Coll Cardiol; Eur Heart J; Circ Res; Cardiovasc Res; Hypertension; Atherosclerosis; Br J Pharmacol; J Appl Physiol; Am J Hypertens; JACC Asia; Mol Cell Life Sci; J Diabetes; J Diabetes Res; Front Cardiovasc Med; Front Pharmacol; Purinergic Signal etc.


    [1] https://ki.se/en/research/kircnet-ki-respiration-and-circulation-network
    [2] https://ki.se/en/research/kiim-ki-inflammation-and-immunology-network
    [3] https://ki.se/en/srp-diabetes/strategic-research-programme-in-diabetes-srp-diabetes

Research

  • Cardiovascular complications are significant clinical challenges in cardiometabolic diseases such as diabetes and obesity, contributing to high morbidity and mortality worldwide. Despite their prevalence, the underlying mechanisms remain poorly understood, and there is a lack of specific therapies and reliable biomarkers to address cardiovascular dysfunction.

    In recent years, our work has revealed that red blood cells (RBCs), traditionally viewed as passive oxygen carriers, undergo dysfunction and act as active mediators of vascular dysfunction. This dysfunction contributes to the development of vascular complications in type 2 diabetes, familial hypercholesterolemia, ST-elevation myocardial infarction, and COVID-19. Targeting these dysfunctional RBCs has emerged as a promising strategy for treating vascular dysfunction.

    RBCs are a rich source of diverse non-coding RNAs (ncRNAs). Through high-throughput profiling and functional validation, using samples from well-characterized clinical cohorts and disease models—including genetically modified animals—our team investigates the expression and functional role of RBC-derived ncRNAs. We explore how alterations in these ncRNAs contribute to cardiovascular complications and their potential as biomarkers and therapeutic targets.

    Additionally, RBCs function as ATP reservoirs, releasing ATP under low oxygen tension. However, this ATP release is impaired in various disease states. A critical focus of our research is understanding the functional interactions between RBCs and the cardiovascular wall, specifically through ATP-mediated purinergic signaling pathways in cardiometabolic diseases and how they respond to hypoxia.

    Our ultimate goal is to identify RBC-derived factors as novel mechanisms driving cardiovascular complications and to establish them as diagnostic markers and therapeutic targets, paving the way for improved clinical outcomes in cardiometabolic diseases.

Articles

All other publications

Grants

  • Swedish Research Council
    1 December 2023 - 30 November 2026
    BackgroundType 2 diabetes (T2D) is an important risk factor for cardiovascular complications. Endothelial dysfunction is a key factor of vascular complications in T2D. We found that erythrocytes (RBCs) undergo dysfunction in T2D which causes endothelial dysfunction. RBCs contain diverse and abundant non-coding (nc)RNAs, of which the expression and function are unknown. We hypothesize that altered function of RBC-derived ncRNAs induces endothelial dysfunction in T2D.AimTo characterize the function of RBC ncRNAs for endothelial dysfunctionTo elucidate how RBC ncRNAs transmit signal to endothelium in T2DTo explore the efficacy of modulating RBC ncRNA as a therapyWork planRBCs are isolated from patients and rodents with T2D as well as healthy controls. ncRNAs are identified via RNA-sequencing and qPCR. ncRNAs are also validated in extracellular vesicles (EVs) released from RBCs. The function of RBC ncRNAs in endothelial dysfunction is examined by co-incubations of RBCs with healthy artery/endothelial cell ex vivo and RBC transfusion rodent model in vivo. The RBC-derived EVs carrying ncRNAs and the signal to the vasculature are determined using molecular, pharmacological and genetic tools. The therapeutic effect of modulating RBC ncRNAs is addressed by determining endothelial function using both patient materials and gene-targeted animals.SignificanceThis study identifies RBC-derived ncRNAs as new disease mechanism and provides new therapy for vascular complication in T2D.
  • 2022 EFSD - NNF Future Leaders Award - Functional role of erythrocyte-derived non-coding RNAs in diabetes-associated vascular complications
    Novo Nordisk Foundation
    1 January 2023 - 31 December 2027
  • Swedish Heart-Lung Foundation
    1 January 2021 - 31 December 2023
  • Swedish Heart-Lung Foundation
    1 January 2020 - 31 December 2022
  • Swedish Research Council
    1 January 2017 - 31 December 2020
  • EFSD/Novo Nordic Foundation Future Leaders Awards

Employments

  • Principal Researcher, Department of Medicine, Karolinska Institutet, 2022-

Degrees and Education

  • Docent, Karolinska Institutet, 2024

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