Corrigendum to "JP4-039 protects chondrocytes from ferroptosis to attenuate osteoarthritis progression by promoting Pink1/Parkin-dependent mitophagy" [J Orthop Transl 51 (2025) 132-144 / doi: 10.1016/j.jot.2025.01.001]

This article is a corrigendum — a formal published correction — to an original research paper investigating whether a compound called JP4-039 can protect joint cartilage cells (chondrocytes) from a form of iron-dependent cell death known as ferroptosis, and whether this protection works by switching on a cellular 'self-cleaning' pathway for damaged mitochondria (Pink1/Parkin-dependent mitophagy). The original study proposed that osteoarthritis, a degenerative joint disease affecting hundreds of millions of people, is worsened when chondrocytes accumulate dysfunctional mitochondria and undergo ferroptosis, and that JP4-039 could interrupt this cascade. Because this record is a corrigendum rather than the primary article, the specific errors being corrected are not detailed in the available abstract or metadata. The underlying science — linking mitochondrial quality control via mitophagy to ferroptosis suppression in chondrocytes — is mechanistically significant, as it positions mitophagy activation as a potential therapeutic strategy for osteoarthritis. Readers should access both the corrigendum and the original 2025 article (DOI: 10.1016/j.jot.2025.01.001) to obtain a complete and accurate account of the reported findings. The correction does not, on its face, invalidate the core hypothesis but may alter specific reported values, figures, or interpretive statements. This entry should be treated as flagging an amended dataset pending full verification against the corrected primary article.

• This is a corrigendum to the original article published in J Orthop Transl 51 (2025) 132-144; specific corrected items are not enumerated in the available metadata and must be retrieved from the full corrigendum text.
• The original study reported that JP4-039 protects chondrocytes from ferroptosis — an iron-dependent, lipid-peroxidation-driven cell death — in the context of osteoarthritis progression, a finding that remains under editorial review pending confirmation of corrected data.
• The proposed mechanism in the original work is promotion of Pink1/Parkin-dependent mitophagy, suggesting that clearing damaged mitochondria reduces the oxidative burden that would otherwise trigger ferroptotic death in joint cartilage cells.

The original study (to which this corrigendum refers) employed an in vitro chondrocyte cell model to investigate the effects of JP4-039, a mitochondria-targeted antioxidant compound, on ferroptosis and Pink1/Parkin-mediated mitophagy. Experimental details including sample sizes, specific induction protocols for ferroptosis, and any in vivo osteoarthritis model components should be verified in the corrected primary article (DOI: 10.1016/j.jot.2025.01.001). As a corrigendum, this record does not itself report new experimental data; methods details here are best-effort reconstructions from the title and citation metadata and carry low confidence.

Because this record is a corrigendum rather than a primary research article, it is not possible to fully evaluate the original study's limitations — including the translational gap between in vitro chondrocyte findings and human osteoarthritis — without reading both documents together. The nature and scope of the correction are unknown from available metadata, meaning that reported effect sizes, mechanistic conclusions, or figure data from the original paper may be materially altered. Future experiments should address whether JP4-039-driven mitophagy activation is sufficient to reduce cartilage degeneration in vivo, and whether the Pink1/Parkin axis is causally required or merely correlative in ferroptosis suppression.

This corrigendum, and the study it corrects, sit within a growing body of work on Pink1/Parkin-dependent mitophagy as a protective mechanism across diverse disease contexts; it extends [§136], which similarly demonstrates that promoting mitophagy suppresses inflammatory cell-death cascades (NLRP3 inflammasome), and parallels [§134], where Pink1/Parkin-linked mitophagy is examined in cardiomyocyte stress — showing that the same pathway can be context-dependently protective or pathological depending on tissue and stimulus. The ferroptosis-mitophagy intersection examined here also conceptually parallels [§124], which targets dysfunctional mitochondria in rheumatoid arthritis via irisin, another musculoskeletal inflammatory disease where mitochondrial quality control is therapeutically relevant. Together, these studies suggest that mitophagy-centered interventions may represent a cross-disease strategy in inflammatory and degenerative musculoskeletal conditions, though the specific corrected data in this corrigendum must be resolved before the JP4-039 findings can be confidently integrated into this mechanistic picture.

• Hirudin Promotes Peripheral Nerve Repair by Enhancing Mitophagy to Suppress NLRP3 Inflammasome Activation
  Directly parallel mechanism: both studies position mitophagy activation as a suppressor of inflammatory/cell-death cascades (NLRP3 vs. ferroptosis), enabling comparison of how mitophagy intersects with distinct downstream death pathways.
• Cardiomyocyte BMAL1 deficiency worsens obesity-related cardiomyopathy with heightened PINK1/Parkin-linked mitophagy and mitochondrial dysfunction
  Shares the specific Pink1/Parkin mitophagy axis as the mechanistic focus, but in cardiomyocytes under obesity-related stress, allowing assessment of whether Pink1/Parkin activation is uniformly protective or tissue-context-dependent.
• Exercise hormone irisin alleviates rheumatoid arthritis by removing dysfunctional mitochondria
  Closest disease-context comparator: targets dysfunctional mitochondria in a different inflammatory joint disease (rheumatoid arthritis), offering a parallel musculoskeletal framework against which to benchmark the osteoarthritis mitophagy findings.
• Dexmedetomidine attenuates LPS-induced acute lung injury via activation of mitochondrial autophagy
  Also examines mitochondrial autophagy activation as a therapeutic strategy in an acute inflammatory injury model (LPS-induced lung injury), providing a mechanistic cross-tissue reference point for evaluating generalizability of mitophagy-directed interventions.