bims-mithem 2026-01-11 papers

Issue of 2026–01–11
three papers selected by
Tim van Tienhoven, Erasmus Medical Center

J Cell Sci. 2026 Jan 01. pii: jcs263847. [Epub ahead of print]139(1):

Mitochondrial dynamics and signaling in stem cell differentiation.

Rahul Kumar Verma, Somya Madan, Richa Rikhy.

Mitochondrial dynamics are defined by the continuous processes of fusion and fission that regulate mitochondrial shape, distribution and activity. They are also involved in cellular functions of mitochondria, such as energy production, metabolic adaptation, apoptosis and cellular stress responses. Consequently, these organelle dynamics play a crucial role in development, growth, differentiation and disease. Mitochondrial morphology is controlled by Drp1 (also known as DNM1L) and Fis1, which drive fission, whereas Opa1, Mfn1 and Mfn2 mediate fusion. The transcription, activation and degradation of these proteins are often regulated by signaling cascades that are crucial for stem cell maintenance and differentiation. In turn, mitochondrial dynamics regulate key outcomes of these pathways. We explore the interplay between mitochondrial fusion and fission proteins and such signaling pathways, including Notch, receptor tyrosine kinase, JNK, Hippo and mTOR signaling, finding that stem cell renewal and differentiation states are dependent on the regulation of signaling pathways by mitochondrial morphology and activity. Overall, this Review highlights how mitochondrial morphology and activity crucially regulate stem cell division for renewal and differentiation, examining their impact across diverse systems.

Keywords: Drp1; Marf; Mfn; Mitochondria; Opa1; Signaling; Stem cells

DOI: https://doi.org/10.1242/jcs.263847

Int J Mol Sci. 2025 Dec 28. pii: 332. [Epub ahead of print]27(1):

Mitochondrial Transplantation Restores Immune Cell Metabolism in Sepsis: A Metabolomics Study.

Tae Nyoung Chung, Se Rin Choi, Su-Hyun Kim, Choong Hwan Lee, Kyuseok Kim.

Sepsis induces severe immune and metabolic dysfunction driven by mitochondrial failure. Mitochondrial transplantation (MT) has emerged as a promising strategy to restore mitochondrial bioenergetics, but its metabolic impact on immune cells remains unclear. Here, we used gas chromatography-time-of-flight mass spectrometry (GC-TOF-MS)-based metabolomics to evaluate metabolic alterations in peripheral blood mononuclear cells (PBMCs) and splenocytes from a rat polymicrobial sepsis model treated with MT. Principal component and partial least-squares discriminant analyses revealed distinct clustering between sham, sepsis, and MT groups. Sepsis markedly suppressed metabolites related to amino acid, carbohydrate, and lipid metabolism, including aspartic acid, glutamic acid, AMP, and myo-inositol, reflecting mitochondrial metabolic paralysis. MT partially restored these metabolites toward sham levels, reactivating tricarboxylic acid (TCA) cycle, nucleotide, and lipid pathways. Pathway analysis confirmed that exogenous mitochondria reversed sepsis-induced metabolic suppression and promoted bioenergetic recovery in immune cells. These findings provide direct metabolomic evidence that MT reprograms immune metabolism and restores oxidative and biosynthetic function during sepsis, supporting its potential as a mitochondrial-based metabolic therapy.

Keywords: energy metabolism; gas chromatography–mass spectrometry; immune cells; metabolomics; mitochondrial dysfunction; mitochondrial transplantation; oxidative phosphorylation; peripheral blood mononuclear cells; sepsis; splenocytes

DOI: https://doi.org/10.3390/ijms27010332