Publications by authors named "M Wlaschek"

The distribution of biomolecules within cells changes upon aging and diseases. To quantitatively determine the spatial distribution of components inside cells, we built the user-friendly open-source 3D-cell-image analysis platform Cell Detection and Analysis of Intensity Lounge (CellDetail). The algorithm within CellDetail is based on the concept of the dipole moment.

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The naked mole-rat (NMR) Heterocephalus glaber (from the Greek/latin words ἕτερος, heteros = divergent, κεφαλή, kephalē = head and glabra = hairless) was first described by Rüppell (Fig. 1) and belongs to the Hystricognath (from the Greek words ὕστριξ, hystrix = porcupine and γνάθος, gnathos = jaw) as a suborder of rodents. NMR are characterized by the highest longevity among rodents and reveal a profound cancer resistance.

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Background: Cellular senescence is the main cause of skin and organ aging and is associated with a wide range of aging-related diseases.

Objectives: To understand which senolytics, senomorphics, and cell-based therapies have been developed to alleviate and even rejuvenate skin aging and reduce cellular senescence.

Methods: Basic literature for the mode of action of senolytics and senomorphics and their clinical perspectives in daily routine are discussed.

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Article Synopsis
  • Severe angiopathy contributes to complications in diabetes, but understanding the mechanisms for effective therapies is lacking.
  • Injecting ABCB5 stromal precursors into diabetic wounds in mice significantly speeds up healing by boosting blood vessel formation through the release of angiogenin.
  • Blocking angiogenin in these precursors slows healing, highlighting its crucial role in tissue repair for diabetic conditions, paving the way for better treatments for nonhealing wounds.
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Fibroblasts residing in the connective tissues constitute the stem cell niche, particularly in organs such as skin. Although the effect of fibroblasts on stem cell niches and organ aging is an emerging concept, the underlying mechanisms are largely unresolved. We report a mechanism of redox-dependent activation of transcription factor JunB, which, through concomitant upregulation of p16 and repression of insulin growth factor-1 (IGF-1), initiates the installment of fibroblast senescence.

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