ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Effects of Cannabidiol on TAFAZZIN-Deficient B-Lymphoblastoid Cells.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Barth Syndrome (BTHS) is a debilitating X-linked genetic disorder caused by mutations in the gene encoding TAFAZZIN, an enzyme responsible for the remodeling of cardiolipin. While cyclic neutropenia is a well-recognized immunological feature of this disease, emerging evidence suggests that lymphopenia may also occur. The objective of this study was to examine the effects of cannabidiol (CBD) on growth, cardiolipin content, and mitochondrial abnormalities in BTHS patient-derived B-lymphoblastoid cells. CBD (1 μM) restored the growth of BTHS B-lymphoblastoids to healthy control levels, but did not alter cell cycle distribution or sub-G1 cell populations, which surprisingly also did not differ from healthy control B-lymphoblastoids. CBD treatment also fully restored the total cellular cardiolipin concentration and reversed the elevation in monolysocardiolipin/cardiolipin ratio in BTHS B-lymphoblastoids to healthy cell levels, but did not restore the cardiolipin fatty acyl composition. Assessment of mitochondrial markers suggested that increased cardiolipin did not result from increased mitochondrial content. This improvement in cardiolipin concentration was associated with a significant increase in the maximal coupled state III respiration of BTHS B-lymphoblastoids, with all five tested BTHS donors exhibiting increased mitochondrial membrane potential following CBD treatment. CBD fully reversed the deficit in succinate dehydrogenase subunit A in BTHS cells, and partially reversed deficits in cytochrome c oxidase subunits I and IV, and partially restored supercomplex I/III
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