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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

  • Leiomodin 1 promotes myogenic differentiation by modulating Sirtuin 1
    Späth* E, C.Schüler* S, Heinze I, Dau T, Minetti A, Hofmann M, von Maltzahn** J, Ori** A
    bioRxiv 2024, https://doi.org/10.1101/2024.03. * equal contribution, ** co-corresponding authors
  • Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia.
    Weinberger T, Denise M, Joppich M, Fischer M, Garcia Rodriguez C, Kumaraswami K, Wimmler V, Ablinger S, Räuber S, Fang J, Liu L, Liu WH, Winterhalter J, Lichti J, Thomas L, Esfandyari D, Percin G, Matin S, Hidalgo A, Waskow C, Engelhardt S, Todica A, Zimmer R, Pridans C, Gomez Perdiguero E, Schulz C
    Elife 2024, 12, RP89377
  • 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
  • Immunofluorescence microscopy on the blood smear identifies patients with myeloproliferative neoplasms.
    Zaninetti C, Vater L, Kaderali L, Crodel CC, Schnöder TM, Fuhrmann J, Swensson L, Wesche J, Freyer C, Greinacher A, Heidel FH
    Leukemia 2024, 38(9), 2051-8

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
  • Human gene-engineered calreticulin mutant stem cells recapitulate MPN hallmarks and identify targetable vulnerabilities.
    Foßelteder J, Pabst G, Sconocchia T, Schlacher A, Auinger L, Kashofer K, Beham-Schmid C, Trajanoski S, Waskow C, Schöll W, Sill H, Zebisch A, Wölfler A, Thomas D, Reinisch A
    Leukemia 2023, 37(4), 843-53
  • Lentiviral in situ targeting of stem cells in unperturbed intestinal epithelium.
    Garside GB, Sandoval M, Beronja** S, Rudolph** KL
    BMC Biol 2023, 21(1), 6 ** co-corresponding authors