Catalina Vasilescu, PhD

@cvasilescu.bsky.social

Biomedical researcher studying mitochondrial disorders. PhD from Anu Suomalainen lab, Helsinki. Postdoc at Prokisch lab, Munich.

@eoscommons.bsky.socialReposted by @cvasilescu.bsky.social

Two already approved drugs, diltiazem and sulbactam, breaking up a mitochondrial protein aggregate and restoring mtDNA replication in a knock-in mouse. Repurposing is the shortest path from mechanism to clinic, though this is still one mutation in one model. Worth following.

@cvasilescu.bsky.social

Crowded epithelia switch from fluid-like motion to a jammed state, preceded by a rise in mitochondrial pyruvate anaplerosis. Limiting mitochondrial pyruvate import kept cells motile and delayed jamming, via RhoA-myosin II and macropinocytosis.

Cell jamming transition is regulated by mitochondrial pyruvate transport and endocytosis. Crowded epithelia switch from fluid-like motion to a jammed state, preceded by a rise in mitochondrial pyruvate anaplerosis. Limiting mitochondrial pyruvate import kept cells motile and delayed jamming, via RhoA-myosin II and macropinocytosis. Bermudez et al., Proc Natl Acad Sci U S A · doi.org/10.1073/pnas.2617216123
@cvasilescu.bsky.social

PEO-linked POLGA mutants are hyperubiquitylated by MITOL and aggregate instead of entering mitochondria. Two approved drugs, diltiazem hydrochloride and sulbactam, disrupt the aggregates, restore mtDNA replication and improve motor performance in a knock-in mouse.

Small molecules rescue pathogenic POLGA aggregation and restore its functions in a mouse model of PEO. PEO-linked POLGA mutants are hyperubiquitylated by MITOL and aggregate instead of entering mitochondria. Two approved drugs, diltiazem hydrochloride and sulbactam, disrupt the aggregates, restore mtDNA replication and improve motor performance in a knock-in mouse. Mohammed et al., EMBO Mol Med · doi.org/10.1038/s44321-026-00532-3
@cvasilescu.bsky.social

The Golgi helps mito fusion. Trans-Golgi vesicles rich in PI(3,4)P2 are recruited to mito fusion sites marked by ER and mitofusin. Without the class II PI3-kinases that make this lipid (PI3K-C2α and β), fusion stalls and mitos fragment, and mice lacking both in cardiomyocytes develop heart failure.

Golgi-derived vesicles containing PI(3,4)P2 drive mitochondrial fusion. Mitochondrial fusion gets help from the Golgi. Trans-Golgi vesicles rich in PI(3,4)P2 are recruited to mitochondrial fusion sites marked by ER and mitofusin. Without the class II PI3-kinases that make this lipid (PI3K-C2α and β), fusion stalls and mitochondria fragment, and mice lacking both in cardiomyocytes develop heart failure. Aki et al., Science · doi.org/10.1126/science.adx9628
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