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@sigtrans-sttt.bsky.social Sep 26, 2026, 3:30 AM

#Fructose directly binds TOM22 and remodels the mitochondrial TOM complex, disrupting protein import, ribosome biogenesis, and #OxidativePhosphorylation, revealing a metabolism-independent mechanism of #Podocyte injury. @tsinghuauniversity.bsky.social

#STTT #OpenAccess: doi.org/10.1038/s413...

Fructose directly remodels the translocase of the outer membrane to impair oxidative phosphorylation in podocytes

@alicefrolov.bsky.social Sep 20, 2026, 5:00 PM

Mitochondrial membrane potential heterogeneity with age

I am sharing a data visualization exploring how mitochondrial membrane potential (Δψm) declines.

#MitochondrialBioenergetics #TMRM #MembranePotential #Mitophagy #SingleCellHeterogeneity #OxidativePhosphorylation #MtDNA
#ProtonMotiveForce

Mitochondrial membrane potential heterogeneity with age

I am sharing a data visualization exploring how mitochondrial membrane potential (Δψm) declines and becomes more dispersed across the lifespan. The figure, titled "Mitochondrial membrane potential collapses and disperses with age," presents single-cell TMRM (tetramethylrhodamine methyl ester) intensity across four age groups in three tissues. I want to emphasize at the outset that the underlying dataset is simulated; it is constructed to illustrate a trend that is well grounded in the existing literature rather than to report novel empirical measurements.

The chart employs a faceted raincloud design, with each tissue occupying its own facet. Within each facet, the four age cohorts are represented by a combination of a half-density (violin) contour, jittered single-cell points, and an overlaid boxplot. This composite format was chosen deliberately to convey both central tendency and the full distributional structure, which is critical here because the phenomenon of interest is not only a shift in the mean but an expansion of intercellular variance.

Two features are salient. First, median TMRM intensity declines monotonically with advancing age across all three tissues, consistent with progressive dissipation of the proton-motive force and diminished electron transport chain coupling efficiency. Second, and more importantly, the distributions broaden with age, indicating increasing cell-to-cell heterogeneity in Δψm. This dispersion is compatible with mosaic accumulation of mtDNA mutations, clonal expansion of dysfunctional mitochondrial populations, and stochastic failure of quality-control mechanisms such as mitophagy.

I would welcome discussion regarding appropriate normalization strategies for TMRM intensity, particularly the non-quench versus quench mode distinction, and how these affect interpretation of the observed variance structure.