M
Mark M. Kockx
Researcher at University of Antwerp
Publications - 159
Citations - 12365
Mark M. Kockx is an academic researcher from University of Antwerp. The author has contributed to research in topics: Apoptosis & Macrophage. The author has an hindex of 55, co-authored 153 publications receiving 11076 citations.
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Journal ArticleDOI
Apoptosis in the Atherosclerotic Plaque Quantitative and Qualitative Aspects
TL;DR: Although both smooth muscle cells and macrophages within the human fatty streaks become susceptible to apoptosis, additional factors are necessary to terminate the cell death pathway, and the TUNEL technique should be combined with additional techniques, such as markers of transcription and morphological criteria.
Journal Article
RNA synthesis and splicing interferes with DNA in situ end labeling techniques used to detect apoptosis.
TL;DR: It is thought that the TUNEL technique should be combined with additional techniques, such as markers of transcription and morphological criteria, as these contain a far greater degree of DNA fragmentation than non-apoptotic nuclei.
Journal ArticleDOI
Epidermal differentiation does not involve the pro-apoptotic executioner caspases, but is associated with caspase-14 induction and processing.
Saskia Lippens,Mark M. Kockx,Michiel W.M. Knaapen,Laurent Mortier,Renata Polakowska,A Verheyen,Maria Garmyn,An Zwijsen,Pierre Formstecher,Danny Huylebroeck,Peter Vandenabeele,Wim Declercq +11 more
TL;DR: Observations strongly suggest that caspase-14 is involved in the keratinocyte terminal differentiation program leading to normal skin cornification, while the executioner caspases are not implicated.
Journal ArticleDOI
Phagocytosis and Macrophage Activation Associated With Hemorrhagic Microvessels in Human Atherosclerosis
Mark M. Kockx,Kristel M. Cromheeke,Michiel W.M. Knaapen,Johan Bosmans,Guido R.Y. De Meyer,Arnold G. Herman,Hidde Bult +6 more
TL;DR: Focal intraplaque microhemorrhages initiate platelet and erythrocyte phagocytosis, leading to iron deposition, macrophage activation, ceroid production, and foam cell formation, and neovascularization can thus promote focal plaque expansion when microvessels become thrombotic or rupture prone.
Journal ArticleDOI
Induction of Atherosclerotic Plaque Rupture in Apolipoprotein E−/− Mice After Adenovirus-Mediated Transfer of p53
Jan H. von der Thüsen,Bart J.M. van Vlijmen,Rob C. Hoeben,Mark M. Kockx,Louis M. Havekes,Theo J.C. Van Berkel,Erik A.L. Biessen +6 more
TL;DR: A strategy to promote (thrombotic) rupture of preexisting atherosclerotic lesions using p53-induced lesion remodeling is described to delineate the processes that precede rupture and to evaluate plaque-stabilizing therapies.