bims-mithem Biomed News
on Mitochondria in Hematopoiesis
Issue of 2026–05–24
two papers selected by
Tim van Tienhoven, Erasmus Medical Center
  1. Mitochondrial Metabolism and Dynamics in Cancer Cells.
  2. Cytotoxic and genotoxic stress transiently increase the contribution of platelet-biased hematopoietic stem cells to platelet production.
  1. Cancer Treat Res. 2026 ;195 109-120
    Mitochondrial Metabolism and Dynamics in Cancer Cells.
    Pedram Fadavi, Farzad Taghizadeh-Hesary.
      Cancer metabolism has long been interpreted through Otto Warburg's original observation that malignant cells favor aerobic glycolysis due to defective mitochondria. Although foundational, this view is now recognized as incomplete. Contemporary evidence demonstrates that mitochondria in cancer cells remain highly functional and play indispensable roles far beyond adenosine triphosphate (ATP) production. Many tumors actively engage mitochondrial oxidative phosphorylation (OXPHOS) alongside glycolysis, enabling metabolic flexibility across the heterogeneous tumor microenvironment (TME). Mitochondria also generate reactive oxygen species (ROS) that stabilize hypoxia-inducible factor-1 (HIF-1), reinforcing pathways that promote angiogenesis, invasion, and survival under hypoxic stress. Beyond bioenergetics and redox regulation, mitochondria critically shape cancer progression through calcium homeostasis and dynamic remodeling. Meanwhile, mitochondrial fusion and fission govern organelle quality control and functional redistribution. Fusion sustains OXPHOS and cancer stem cell quiescence, whereas fission promotes proliferation, migration, immune evasion, and therapy resistance. Collectively, these findings establish mitochondria as central regulators of tumor evolution, influencing survival in the TME, immune escape, malignant upgrading, and resistance to chemotherapy, radiotherapy, and immunotherapy. Understanding mitochondrial biology, therefore, provides essential insight into cancer progression and reveals promising therapeutic opportunities.
    Keywords:  ATP; Calcium homeostasis; Cancer; Mitochondria; Mitochondrial dynamics
    DOI:  https://doi.org/10.1007/978-3-032-21861-2_6
  2. Exp Hematol. 2026 May 17. pii: S0301-472X(26)00089-5. [Epub ahead of print] 105456
    Cytotoxic and genotoxic stress transiently increase the contribution of platelet-biased hematopoietic stem cells to platelet production.
    Yiran Meng, Xiying Ren, Rong Li, Bowen Zhang, Claus Nerlov.
      Platelets are produced via a canonical pathway emanating from multi-lineage hematopoietic stem cells (ML-HSCs), and a faster, direct pathway used by platelet-biased (P-)HSCs where the latter circumvents progenitors intermediate between HSCs and megakaryocytes. However, the physiological role of these distinct pathways remains to be determined. Here, we use Vldlr-iCre lineage tracing to identify platelets originating from platelet-biased HSCs, and to show that P-HSC contribution to the megakaryocyte progenitor (MkP) population and platelet production is increased after 5-fluorouracil or cyclophosphamide treatment, where proliferating progenitors are severely depleted. In contrast, antibody-mediated platelet depletion, which leaves the progenitor hierarchy intact, did not increase the proportion of platelets generated by P-HSCs. Therefore, P-HSCs provide rapid platelet reconstitution without the need for complete re-establishment of the progenitor hierarchy after cytotoxic and genotoxic challenges due to their ability to more rapidly generate megakaryocyte progenitors from HSCs. Teaser Abstract: The study shows that platelet-biased hematopoietic stem cells (P-HSCs) provide a rapid pathway for platelet production that bypasses intermediate progenitors. Using a Vldlr-iCre lineage-tracing mouse model, the authors demonstrate that this direct pathway becomes significantly more active after cytotoxic or genotoxic stress (e.g., 5-FU or cyclophosphamide), when platelet progenitors are depleted. In contrast, simple platelet depletion without progenitor damage does not increase P-HSC contribution. Thus, P-HSCs accelerate platelet recovery after stress by rapidly generating megakaryocyte progenitors, supporting a specialized physiological role in emergency thrombopoiesis.
    DOI:  https://doi.org/10.1016/j.exphem.2026.105456
This page is being maintained by Thomas Krichel. It was last updated on 2026‒05‒26 at 7:32.