Mitochondrial research library

A careful comparison of public POLG astrocyte papers shows that mitophagy, autophagy-flux and reactive-astrocyte readouts should not be treated as one rescue signal.

A public Twinkle helicase workbook can support aggregate pause comparisons, but not same-molecule pause-state modeling without trace identifiers.

Lactate and pyruvate are more than exercise byproducts, but they are not stand-alone mitochondrial treatments.

A source-coded working paper asks when POLG liver evidence should be interpreted as a stress-and-regeneration problem rather than ordinary liver failure context.

A POLG-focused working paper asks when vascular-cell studies need transfer controls before calling a finding cell-autonomous.

A careful reading of CD8 T cell studies separates ex vivo MPC inhibition from tumor-site lactate use.

A synthetic POLG model asks which measurements can identify hidden assembly and loss rates.

A careful evidence map of mitochondrial calcium uptake in muscle.

A cautious research framework for judging mitochondrial build-and-clear claims in TWNK-related disease biology.

A bounded review of how exercise relates to mitochondria in older muscle.

Exercise can use short-lived oxidant signals as part of mitochondrial adaptation, so antioxidant trial results need endpoint-specific interpretation.

Mitochondrial transfer may help injured cells in narrow settings, but evidence does not yet show general organelle replacement.

A working paper explains how RNA escaping from stressed mitochondria can act as an inflammatory signal in senescent cells.

Lactate and pyruvate are frequently treated as interchangeable three-carbon fuels in discussions of mitochondrial biogenesis, yet primary studies indicate that monocarboxylate identity, transport context, redox handling, post-translational signaling, compartment, and PGC-1alpha dependence can separate mitochondrial adaptation into distinct routes. This working paper evaluates a two-route monocarboxylate-control model across skeletal-muscle cells, mouse skeletal muscle, human exercise biopsies, hippocampal lactate-transport experiments, cardiac mitochondrial lactate-import experiments, lactate electron-transport-chain signaling experiments, skeletal-muscle mitochondrial-pyruvate-carrier perturbation, live-cell lactate/pyruvate imaging, and 2026 lactylation-linked PGC-1 studies.

A plain-language look at how two common cellular fuels—lactate and pyruvate—may change the way muscle cells build, use, and measure mitochondria.

This paper formulates a mitochondrial-constrained organ-game framework in which organ subsystems adopt locally regulated strategies, interact through shared resources and signals, and occupy metastable macrostates. Its main contribution is an identification and falsification program linking mitochondrial reserve, threshold geometry, recovery, and regime selection.

AlphaGenome was applied to five participant-provided variants in POLG, TWNK, and MTHFR. The exploratory profiles distinguish protein-centered predictions from secondary regulatory hypotheses but do not establish pathogenicity, clinical severity, or causal effects on energy production.

Initial internal construct validation of the Mito Map Energy Score against a separately recorded composite of grip strength, five-times sit-to-stand performance, baseline fatigue, and post-task fatigue. The primary pipeline-defined analysis included 21 participants.

This manuscript proposes a paired tumor-host bioenergetic phenotyping framework connecting tumor mitochondrial phenotype, host functional phenotype, treatment exposure, and clinically important tumor and host outcomes. The framework is intended to motivate collaborative validation and actionable care pathways, not to claim that the Energy Score is itself a direct mitochondrial assay.