Thomas Thum
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Explore the profile of Thomas Thum including associated specialties, affiliations and a list of published articles.
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463
Citations
22373
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Recent Articles
1.
Ghigo A, Ameri P, Asnani A, Bertero E, de Boer R, Farmakis D, et al.
Eur J Heart Fail
. 2025 Mar;
PMID: 40069106
New anticancer therapies with potential cardiovascular side effects are continuously being introduced into clinical practice, with new and often unexpected toxicities becoming apparent only after clinical introduction. These unknown toxicities...
2.
Stojanovic S, Thum T, Bauersachs J
Cardiovasc Res
. 2025 Mar;
PMID: 40036821
Accumulation of senescent cells is an increasingly recognized factor in the development and progression of cardiovascular disease. Senescent cells of different types display a pro-inflammatory and matrix remodeling molecular program,...
3.
Hess A, Renko A, Schafer A, Jung M, Fraccarollo D, Schmitto J, et al.
Mol Imaging Biol
. 2025 Mar;
PMID: 40029570
Purpose: Myocardial infarction (MI) triggers complex cellular responses essential for tissue repair and remodeling, including myofibroblast activation. Fibroblast activation protein alpha (FAP) identifies activated myofibroblasts post-MI, however its spatial distribution...
4.
Waleczek F, Cipriano G, Haas J, Garg A, Pfanne A, Just A, et al.
Int J Mol Sci
. 2025 Jan;
26(1.
PMID: 39796086
Ischemic heart disease is the leading cause of death worldwide. Reduced oxygen supply and myocardial hypoxia lead to tissue damage and impairment of the heart function. To the best of...
5.
6.
Elliott P, Schunkert H, Bondue A, Behr E, Carrier L, van Duijn C, et al.
Eur Heart J
. 2024 Dec;
46(4):344-353.
PMID: 39673718
In the modern era, cardiologists managing patients and families with cardiomyopathies need to be familiar with every stage of the diagnostic pathway from clinical phenotyping to the prescription and interpretation...
7.
Weber N, Montag J, Kowalski K, Iorga B, de la Roche J, Holler T, et al.
J Mol Cell Cardiol
. 2024 Dec;
198():112-125.
PMID: 39647438
Hypertrophic Cardiomyopathy (HCM) is often caused by heterozygous mutations in β-myosin heavy chain (MYH7, β-MyHC). In addition to hyper- or hypocontractile effects of HCM-mutations, heterogeneity in contractile function (contractile imbalance)...
8.
Targeting fibroblast phenotype switching in cardiac remodelling as a promising antifibrotic strategy
Kel A, Thum T, Kunduzova O
Eur Heart J
. 2024 Nov;
46(4):354-358.
PMID: 39582108
Myocardial fibrosis, a common feature of heart disease, remains an unsolved clinical challenge. Fibrosis resolution requires activation of cardiac fibroblasts exhibiting context-dependent beneficial and detrimental dichotomy. Here, we explored the...
9.
Van Linthout S, Stellos K, Giacca M, Bertero E, Cannata A, Carrier L, et al.
Eur J Heart Fail
. 2024 Nov;
27(1):5-25.
PMID: 39576264
Gene therapy has recently become a reality in the treatment of cardiovascular diseases. Strategies to modulate gene expression using antisense oligonucleotides or small interfering RNA are proving to be safe...
10.
Borisch C, Thum T, Bar C, Hoepfner J
J Transl Med
. 2024 Oct;
22(1):965.
PMID: 39449071
Fabry disease is a multi-organ disease, caused by mutations in the GLA gene and leading to a progressive accumulation of glycosphingolipids due to enzymatic absence or malfunction of the encoded...