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Published Erratum
. 2026 Feb 3;123(5):e2600337123.
doi: 10.1073/pnas.2600337123. Epub 2026 Jan 29.

Correction for Hou et al., Therapeutic restoration of mitochondria-endoplasmic reticulum cross talk for osteoarthritis

No authors listed
Published Erratum

Correction for Hou et al., Therapeutic restoration of mitochondria-endoplasmic reticulum cross talk for osteoarthritis

No authors listed. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Fig. 4.
Fig. 4.
SIRT3 promotes mitochondrial fusion through MFN2 deacetylation. (A) Representative fluorescence and TEM images of mitochondria in chondrocytes treated with AAV-SIRT3 or siSIRT3. (B) Mitochondrial aspect ratio of mitochondria in chondrocytes (n = 80). (C) Measurement of mitochondrial branch length in chondrocytes (n = 400). (D and E) Representative images and quantitative analysis of mitochondrial membrane potential (n = 8). (F–H) OCR, ATP production, and maximal respiration measured by the XFe96 Seahorse Analyzer (n = 4). (I) Representative images of Safranin O/Fast Green staining and immunofluorescence for MFN2 in mice. (J) Quantitative analysis of MFN2-positive cells (n = 6). (K) Translational expression levels of extracellular matrix metabolism markers. (L) Translational expression levels of mitochondrial dynamics markers. (M) Molecular docking analysis of SIRT3 and MFN2 interaction. (N–Q) Coimmunoprecipitation assays validating the interaction between SIRT3 and MFN2. (R and S) Effects of SIRT3 on the acetylation level of MFN2. (T) The deacetylation site “K560” on MFN2 across several species. All samples were obtained at 8 wk after surgery. The mice in the sham group were selected to be fed with mice of the same age as the DMM group, and samples were taken when the mice were all 16 wk old. Data are shown as means ± SDs and statistical significance is analyzed by one-way ANOVA. Sta- tistically significant differences are indicated by P < 0.05 between the indicated groups.
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