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Home>Research>Subarea 4: Cell Dynamics and Molecular Damages in Aging
Research focus of Subarea 4.

Subarea 4: Cell Dynamics and Molecular Damages in Aging

The research focus of Subarea 4 is on studying damages of macromolecules (proteins, nucleic acids) and determining the structure-function relationship of biomolecules relevant to damage and damage repair processes and responses to molecular damage that might lead to aging and aging-associated pathologies.

The studies are focused on the following research areas: DNA replication, DNA damage responses (DDR), stress responses, metabolic stresses, protein trafficking and protein damages.

The research is defined by four focus areas:

  • DNA damage response in tissue homeostasis and neuropathies,
  • Quality control in the endoplasmic reticulum for secretory pathway in aging processes,
  • Intrinsic and extrinsic factors implicated in cellular decline during aging, and
  • DNA replication and genomic integrity preventing premature aging and diseases.

Research focus of Subarea 4.

The accumulation of damaged macromolecules or subcellular organelles is associated with dysfunction of a cell, which contributes to tissue & organ failure. DNA damage, genomic instability, protein misfolding or defects in toxic protein degradation can compromise cell functionality. Alterations of mitochondrial DNA and protein complexes affect cellular metabolism, which will have a general impact on cell integrity.

Publications

(since 2016)

2025

  • Attenuated growth factor signaling during cell death initiation sensitizes membranes towards peroxidation.
    Gollowitzer A, Pein H, Rao Z, Waltl L, Bereuter L, Loeser K, Meyer T, Jafari V, Witt F, Winkler R, Su F, Große S, Thürmer M, Grander J, Hotze M, Harder S, Espada L, Magnutzki A, Gstir R, Weinigel C, Rummler S, Bonn G, Pachmayr J, Ermolaeva M, Harayama T, Schlüter H, Kosan C, Heller R, Thedieck K, Schmitt M, Shimizu T, Popp J, Shindou H, Kwiatkowski M, Koeberle A
    Nat Commun 2025, 16(1), 1774
  • Neuronal autophagy in the control of synapse function.
    Karpova A, Hiesinger PR, Kuijpers M, Albrecht A, Kirstein J, Andres-Alonso M, Biermeier A, Eickholt BJ, Mikhaylova M, Maglione M, Montenegro-Venegas C, Sigrist SJ, Gundelfinger ED, Haucke V, Kreutz MR
    Neuron 2025, 113(7), 974-90
  • DNA damage response regulator ATR licenses PINK1-mediated mitophagy.
    Marx* C, Qing* X, Gong* Y, Kirkpatrick J, Siniuk K, Beznoussenko GV, Kidiyoor GR, Kirtay M, Buder K, Koch P, Westermann M, Bruhn C, Brown EJ, Xu X, Foiani M, Wang ZQ
    Nucleic Acids Res 2025, 53(5), gkaf178 * equal contribution
  • Genetic- and culture-based tools for studying Bacteroides fragilis.
    Schnizlein MK, Dubey AA, Fiebig A, Crosson S
    Microbiol Resour Announc 2025 (epub ahead of print)

2024

  • Correction: IER3IP1-mutations cause microcephaly by selective inhibition of ER-Golgi transport.
    Anitei M, Bruno F, Valkova C, Dau T, Cirri E, Mestres I, Calegari F, Kaether C
    Cell Mol Life Sci 2024, 81(1), 465
  • IER3IP1-mutations cause microcephaly by selective inhibition of ER-Golgi transport.
    Anitei M, Bruno F, Valkova C, Dau T, Cirri E, Mestres I, Calegari F, Kaether C
    Cell Mol Life Sci 2024, 81(1), 334
  • Hormesis as an adaptive response to infection.
    Bauer M, Ermolaeva M, Singer M, Wetzker R, Soares MP
    Trends Mol Med 2024, 30(7), 633-41
  • Analysis of the role of YIPF5 in the secretory pathway and microcephaly
    Bruno F
    Dissertation 2024, Jena, Germany
  • The Aging Synapse: An Integrated Proteomic And Transcriptomic Analysis
    Caterino* C, Ugolini* M, Durso W, Jevdokimenko K, Groth M, Riege K, Görlach M, Fornasiero E, Ori A, Hoffmann S, Cellerino A
    bioRxiv 2024, https://doi.org/10.1101/2024.12. * equal contribution
  • Too old for healthy aging? Exploring age limits of longevity treatments.
    Chaudhari PS, Ermolaeva MA
    NPJ Metab Health Dis 2024, 2(1), 37