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Research focus of Subarea 1.

Subarea 1: Stem Cell Aging

The individual research groups within Subarea 1 investigate the causes and consequences of stem cell aging. The research work spans from basic model organisms over genetic mouse models up to humanized mouse models engrafted with human stem cells.

According to the FLI, with the closure of two groups since 2016 the representation of invertebrate models of stem cell research was reduced in Subarea 1. The institute presumes that the recruitment of new groups should fill this gap.

The research is defined by four focus areas:

  • Cell-intrinsic mechanisms limiting the function of aging stem and progenitor cells,
  • Aging-associated alterations of stem cell niches and the systemic environment,
  • Mechanisms of clonal selection and epigenetic drifts in stem cell aging, and
  • Microbiota- and metabolism-induced impairments in stem cell function during aging (in context of the new focus area Microbiota and Aging currently being built up within Subarea 2).

Research focus of Subarea 1.

a) It is currently not well understood what mechanisms impair cellular functions in aging. b) The relative contribution of niche cells and systemic acting factors on stem cell aging have yet to be determined in different tissues. c) Clonal expansion of mutant cells associates with disease development in aging humans. Mechanistically, the process remains poorly understood. Changes in color intensity depict clonal dominance originating from stem (green) or progenitor cells (gray). d) Emerging evidences indicate that aging associated alterations in microbiota influence stem cell function and vice versa.

Publications

(since 2016)

2024

  • Imetelstat-mediated alterations in fatty acid metabolism to induce ferroptosis as a therapeutic strategy for acute myeloid leukemia.
    Bruedigam C, Porter AH, Song A, Vroeg In de Wei G, Stoll T, Straube J, Cooper L, Cheng G, Kahl VFS, Sobinoff AP, Ling VY, Jebaraj BMC, Janardhanan Y, Haldar R, Bray LJ, Bullinger L, Heidel FH, Kennedy GA, Hill MM, Pickett HA, Abdel-Wahab O, Hartel G, Lane SW
    Nat Cancer 2024 (epub ahead of print)
  • Denervation alters the secretome of myofibers and thereby affects muscle stem cell lineage progression and functionality.
    Henze H, Hüttner SS, Koch P, Schüler SC, Groth M, von Eyss B, von Maltzahn J
    NPJ Regen Med 2024, 9(1), 10
  • CRISPR/Cas9-Mediated Modification of PTP Expression.
    Lossius C, Kresinsky A, Quiet L, Müller JP
    Methods Mol Biol 2024, 2743, 43
  • Vitamin B3 Containing Polymers for Nanodelivery.
    Mapfumo PP, Solomun JI, Becker F, Moek E, Leiske MN, Rudolph LK, Brendel JC, Traeger A
    Macromol Biosci 2024 (epub ahead of print)
  • Consequences of GMPPB deficiency for neuromuscular development and maintenance.
    Schurig MK, Umeh O, Henze* H, Jung* MJ, Gresing L, Blanchard V, von Maltzahn J, Hübner* CA, Franzka* P
    Front Mol Neurosci 2024, 17, 1356326 * equal contribution
  • Aggregates of nonmuscular myosin IIA in erythrocytes associate with GATA1- and GFI1B-related thrombocytopenia.
    Zaninetti C, Rivera J, Vater L, Ohlenforst S, Leinøe E, Böckelmann D, Freson K, Thiele T, Makhloufi H, Rath M, Eberl W, Wolff M, Freyer C, Wesche J, Zieger B, Felbor U, Heidel FH, Greinacher A
    J Thromb Haemost 2024, 22(4), 1179-86

2023

  • Evolution, mechanism and limits of dietary restriction induced health benefits and longevity.
    Becker F, Behrends MM, Rudolph KL
    Redox Biol 2023, 63, 102725
  • Genetic separation of chronic myeloid leukemia stem cells from normal hematopoietic stem cells at single-cell resolution.
    Chen Y, Möbius S, Riege K, Hoffmann S, Hochhaus A, Ernst* T, Rudolph* KL
    Leukemia 2023, 37(7), 1561-6 * equal contribution
  • A YIPF5-GOT1A/B complex directs a transcription-independent function of ATF6 in ER export
    Cramer P, Yonemura Y, Behrendt L, Marszalek A, Sannai M, Durso W, Günes C, Szafranski K, Nakamura N, Nasrashvili T, Mayer J, von Eyss** B, Kaether** C
    bioRxiv 2023, 10.1101/2023.12.12.569033 ** co-corresponding authors
  • Cell fate determinant Llgl1 is required for propagation of acute myeloid leukemia.
    Eifert T, Hsu CJ, Becker AL, Graessle S, Horne A, Bemmann F, Zhang Q, Heuser M, Vasioukhin V, Scholl S, Hochhaus A, Siegerist F, Endlich N, Bullinger L, Lane SW, Haas S, Schnoeder TM, Heidel FH
    Leukemia 2023, 37(10), 2027-35