Clauss Lab

The research lab of Matthias Clauss, PhD, is focused on vascular function and repair are involved in many diseases, in particular in those of the cardiopulmonary system. The research program in this lab is concerned with the mechanisms of vascular endothelial cell activation and aims to identify the links between aging, chronic inflammation and infection in blood vessel function and repair. A specific focus is on the regulation of proangiogenic endothelial progenitor cells (ECFC) and anti-angiogenic factors such as EMAP II.


Active Research

NIH funding including 1R01HL154859-02 (Clauss/ Potential Role of Extracellular Vesicles for the Development of HIV Comorbidities/ 1/2020-7/31/2024)

1R01HL152804-02 (MacLean/ Exploratory Research on HIV Contribution to Heart and Lung Comorbidities/ 4/1/2020-2/29/2024)

R21AG074179 (Wang/ The Role of COVID-19 Endothelial Cell Dysfunction and Hypercoagulability in the Development of Post-ICU Cognitive Impairment and Dementia/ 01/01/2022 - 12/31/2023)

  • HIV-1 Infection and Premature Aging
    HIV-1 infection can cause increased risk for cardiovascular and pulmonary diseases. In HIV-1 studies researchers in the Clauss lab have identified an intracellular protein, HIV-Nef, as a likely candidate for cardiovascular and pulmonary disease development, even in the presence of anti-retroviral drugs. Noteworthy, these scientists are the first to demonstrate that HIV-Nef protein (!) levels in extracellular vesicles (EV) from un-treated patients are comparable to levels found in anti-retroviral drug treated patients (In collaboration with Homer L. Twigg III). Interestingly HIV-Nef can induce premature aging in endothelial cells, potentially explaining increased comorbidity risks in people living with HIV. In analogy to HIV, we hypothesize that long COVID-19 is caused by EV-associated inflammatory load (EVAIL) as summarized in our “EVAIL" review article.
  • Pro-Apoptotic EMAP II, a Pulmonary Disease Accelerator
    Research on the pro-apoptotic EMAP II culminated in the development of a humanized EMAP II neutralizing antibody as therapeutic tool for treating pulmonary hypertension, cigarette smoke induced emphysema and Influenza-A-induced lung injury. Sponsored by three awards (DoD, NIH-SBIRphaseII and NIH-STTR; PI Clauss for Allinaire), this neutralizing antibody is currently advancing towards IND approval for clinical trials for pulmonary hypertension (In partnership with Chiesi Farmaceutici S.p.A.)
  • Premature Aging of Endothelial Stem Cells ECFC
    To understand the role of pro-inflammatory and infectious agents in premature aging of endothelial stem cells like progenitor cells (ECFC). The Clauss Lab team was the first to demonstrate that oxidative stress and cytokines cause premature aging (senescence) in these ECFC (Zhang et al., FASEB Journal 2009) and identified tmTNF as a  protective mechanism against this senescence (Green et al., Circulation Research 2016). These scientists are currently studying ECFC stem cells in small rodents including rat and transgenic mouse models (In collaboration with Merv Yoder, David Basile, Laura Haneline and Tim Lahm).

Research Team Members

From left to right: Mariola Bednorz (visiting scientist), Matthias Clauss (PI), Noelle Dahl (research analyst), Sarvesh Chelvanambi (PhD student) and Jithin Kuriakose (MS student).