Viral Mitochondriopathy in COVID-19  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), disrupts cellular mitochondria, leading to widespread chronic inflammation and multi-organ dysfunction. Viral proteins cause mitochondrial bioenergetic collapse, disrupt mitochondrial dynamics, and impair ionic homeostasis, while avoiding antiviral defenses, including mitochondrial antiviral signaling. These changes drive both acute COVID-19 and its longer-term effects, known as “long COVID”. This review examines new findings on the mechanisms by which SARS-CoV-2 affects mitochondria and for the impact on chronic immunity, long-term health risks, and potential treatments. Highlights SARS-CoV-2 disrupts mitochondria, impairing energy production and releasing mtDNA. Viral proteins block the MAVS pathway, reducing interferon responses. Disrupts metabolism, enhances glycolysis and lipid storage, impedes immune function. Damaged mitochondria activate inflammasomes, raising inflammation. Mitochondrial-targeted therapies may reduce COVID-19 severity and long-term effects.   Published (Sept. 2025) in redox Biology: https://doi.org/10.1016/j.redox.2025.103766

Viral proteins, including ORF9b and ORF10, cause mitochondrial bioenergetic collapse, disrupt mitochondrial dynamics, and impair ionic homeostasis. SARS-CoV-2 infection also interferes with the mitochondrial antiviral signaling leading to increased viral replication #Covid19 #immunity #mitochodria

MitoTracker transfers from astrocytes to neurons independently of mitochondria The neuroprotective transfer of mitochondria from astrocytes to neurons has been primarily investigated by labelling astrocytic mitochondria with the dye MitoTracker. Here we report that MitoTracker transfers to neurons from both astrocytes and astrocyte-conditioned media, independently of mitochondrial transfer. Our observations should prompt an essential re-evaluation of the literature concerning astrocyte-neuron mitochondrial transfer and in other systems in which contact-independent transfer has been observed using mitochondrial dyes. ### Competing Interest Statement The authors have declared no competing interest. MSD (United Kingdom), https://ror.org/004nn4n27, PRJ_20446 DEVINE MSD MRC The Francis Crick Institute, https://ror.org/04tnbqb63, CC2206

Wow!
Is (some of) the literature on #mitochodria transfer via #tunnelingnanotubes simply an artefact of mitotracker transfer?

www.biorxiv.org/content/10.1...

#EndothelialCell #Mitochodria #LimbIschemia #EndMT

Thrilled to have played a small role in this exciting story😀

Integrated single-cell RNA-seq analysis reveals mitochondrial calcium signaling as a modulator of endothelial-to-mesenchymal transition

#ScienceAdv 2024
www.science.org/doi/10.1126/...