Study type: In vivo/preclinical · Status: Verified against declared source

SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome.

Scientific reports · 2024

Study scale: Transmission Electron Microscopy (TEM) analysis of mitochondrial morphology.

Product or molecular entity relationships

SS-31: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.

Plain-language verified summary

Question

Cardiac isolated mitochondria were sedimented by centrifugation at 10,000×g for 10 min at 4 °C, the supernatant was removed, and the resulting pellet was fixed in 2.5% glutaraldehyde 0.1 M phosphate buffer (TBS) for 1 h at 4 °C.

Methods

Not reported in the reviewed source.

Scale or participants

Transmission Electron Microscopy (TEM) analysis of mitochondrial morphology.

Key findings

Barth syndrome (BTHS) is a lethal rare genetic disorder, which results in cardiac dysfunction, severe skeletal muscle weakness, immune issues and growth delay.

Limitations and uncertainty

The immunoblot analysis of DRP1 in TazKD heart homogenates displayed high variability in total DRP1 protein level with no significant differences compared to Wt (Fig.

Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.