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Lillemor Mattsson Hulten

Professor, adjungerad

Lillemor Mattsson Hulten
Professor, adjungerad
Lillemor.Mattsson@wlab.gu.se

Postal Address: Su sahlgrenska, 41345 Göteborg
Visiting Address: Wallenberglab/su , 41345 Göteborg


Department of Molecular and Clinical Medicine at Institute of Medicine (More Information)
SU Sahlgrenska
413 45 Göteborg
Fax: +46 31823762
Visiting Address: Blå stråket 5 B Wallenberglab/SU , 413 45 Göteborg

About Lillemor Mattsson Hulten

Professor, adjunct, PhD, Principal Investigator
Lillemor Mattsson Hultén focuses on the role of ischemia-induced lipid accumulation and inflammation in cardiovascular disease. Her team is especially interested in elucidating the mechanisms underlying ischemia-induced lipoxygenases and inflammatory activation and atherothrombotic events as stroke and ischemic heart disease.

Main research

Despite dramatic advances in recent years, atherosclerotic cardiovascular disease and stroke are still leading causes of morbidity and mortality worldwide. The development of therapies for atherosclerosis requires a thorough understanding of the molecules that are involved in its pathogenesis.


Ischemic stroke and ischemic heart disease share common risk factors and show a similar pathophysiology in terms of atherosclerosis. The exact relationship between lesion development in carotid and coronary arteries and acute events has not been clearly determined, but inflammation is associated with atherosclerotic changes in both types of arteries. Evidence suggests that a systemic inflammatory response plays a role in the destabilization of atherosclerotic lesions, initiating lesion rupture and subsequent thrombosis. We have shown that lipoxygenase products increase platelet aggregation and thrombin generation. The identification of a set of biomarkers to indicate patients at risk of ischemic atherothrombotic events would thus be of great advantage.

Group members

  • Mikael Sandstedt, PhD student, MD
  • Aditi Chaudhari, PhD, Research Associate
  • Victoria Rotter Sopasakis, PhD
  • Joakim Sandstedt, MD, PhD

Funding

Hjärt-Lungfonden, Vetenskapsrådet, ALF-medel.

Key Publications

Mikael Sandstedt, Victoria Rotter Sopasakis, Annika Lundqvist, Kristina Vukusic, Anders Oldfors, Göran Dellgren, Joakim Sandstedt, Lillemor Mattsson Hultén. Hypoxic cardiac fibroblasts from failing human hearts decrease cardiomyocyte calcium peak frequency in an ALOX15/ALOX15B dependent manner. PLoSONE 2018, 13(8): e0202693.

Joakim Sandstedt, Mikael Sandstedt, Annika Lundqvist, Märta Jansson, Anders Jeppsson, Lillemor Mattsson Hultén. Human cardiac fibroblasts isolated from patients with severe heart failure are immune-competent cells mediating an inflammatory response. Cytokine 2019, 213; 319-325.

Rotter Sopasakis V, Sandstedt J, Johansson M, Lundqvist A, Bergström G, Jeppsson A, Mattsson Hultén L. Toll-like receptor-mediated inflammation markers are strongly induced in heart tissue in patients with cardiac disease under both ischemic and non-ischemic conditions. International Journal of Cardiology 2019, 293; 238–247.
 

Latest publications

Deficiency in perilipin 5 reduces mitochondrial function and membrane depolarization in mouse hearts.
Linda Andersson, Christina Drevinge, Ismena Mardani, Knut T Dalen, Marcus Ståhlman et al.
The international journal of biochemistry & cell biology, Journal article 2017
Journal article

Showing 1 - 10 of 66

2019

2018

2017

Deficiency in perilipin 5 reduces mitochondrial function and membrane depolarization in mouse hearts.
Linda Andersson, Christina Drevinge, Ismena Mardani, Knut T Dalen, Marcus Ståhlman et al.
The international journal of biochemistry & cell biology, Journal article 2017
Journal article

2016

Showing 1 - 10 of 66

Page Manager: Karin Allander|Last update: 9/19/2019
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