bims-mitrat 2026-06-07 papers

Cell Metab. 2026 Jun 02. pii: S1550-4131(26)00155-5. [Epub ahead of print]38(6): 1081-1084

Intercellular mitochondrial transfer in disease: Therapeutic opportunity or driver of tumor progression?

Intercellular mitochondrial transfer has emerged as a key mode of metabolic communication across tissues. Its outcomes are context dependent, spanning from therapeutic benefits to pathological risks.

DOI: https://doi.org/10.1016/j.cmet.2026.04.017

Cell Transplant. 2026 Jan-Dec;35:35 9636897261453307

Mitochondrial transplantation as an immunomodulatory strategy: Modulating polymorphonuclear leukocytes for functional tissue regeneration.

Samantha C Hall, Evan N Main, Gary L Bowlin.

Following biomaterial implantation, modulation of the acute immune response is essential for tissue regeneration. Polymorphonuclear leukocytes (PMNs) are critical effector cells in wound healing, and PMN dysfunction is mediated by mitochondrial dysfunction and can lead to prolonged inflammation and tissue damage. It was hypothesized that mitochondrial transplantation could be applied to PMNs in pro-inflammatory states as a means of upregulating regenerative proteins. Primary human PMNs were isolated from donor blood. Isolated PMNs and exogenous mitochondria were co-incubated to induce mitochondrial transplantation. Resulting interactions were assessed through microscopy to confirm initial uptake and mitochondria membrane potential retention, intracellular reactive oxygen species (ROS) analyses (n = 5), and PMN secretome quantification (n = 10) using multiplex protein analysis. Human PMNs were able to successfully uptake delivered mitochondria, and regenerative factors essential for tissue repair and immune cell recruitment including fibroblast growth factor-2 (FGF-2), interleukin (IL)-22, monocyte chemoattractant protein-1 (MCP-1), and granulocyte colony-stimulating factor (G-CSF) were significantly upregulated, indicating that exogenous mitochondria represent promising modulators of PMN function with broad clinical potential.

Keywords: host-biomaterial response; immunoengineering; mitochondrial transplantation; polymorphonuclear leukocyte; tissue regeneration

DOI: https://doi.org/10.1177/09636897261453307

Mech Ageing Dev. 2026 Jun 01. pii: S0047-6374(26)00058-8. [Epub ahead of print] 112206

Cell-specific energy crisis in the ageing brain: Mitochondrial dynamics drives neuron-glia metabolic uncoupling and neurodegeneration.

Kai Wang, Yongchao Liu, Haojia Zhang, Xiaomin Li, Rui Zhou, Wei Shao, Zijin Sun.

Ageing is the primary risk factor for neurodegeneration and age-related cognitive decline, which is increasingly recognised as a systemic collapse of metabolic crosstalk between neurons and glial cells in the brain. This narrative review elucidates that mitochondrial dynamics - encompassing biogenesis, fusion, fission, and mitophagy - acts as the core regulatory mechanism governing this multicellular interaction network, and drives the cell-specific energy crisis that underpins pathological progression in the ageing brain. We delineate that senescent astrocytes disrupt the astrocyte-neuron lactate shuttle, oligodendrocytes develop ATP deficits triggering myelin breakdown, and microglia undergo maladaptive immunometabolism and metabolic reprogramming via excessive Drp1-mediated mitochondrial fission, which collectively initiates and amplifies chronic neuroinflammation and neurodegenerative damage. Crucially, we highlight intercellular mitochondrial transfer as a vital endogenous rescue mechanism, wherein glial cells donate functional mitochondria to stressed neurons to mitigate damage. Finally, we synthesise emerging therapeutic strategies targeting the glia-neuron mitochondrial social network, providing a holistic framework for restoring brain bioenergetic homeostasis and delaying age-related neurodegenerative progression.

Keywords: Cell-Specific Energy Crisis; Immunometabolism; Intercellular Mitochondrial Transfer; Metabolic Reprogramming; Mitochondrial Dynamics

DOI: https://doi.org/10.1016/j.mad.2026.112206