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. 2026 Jul 28;17:1930236. doi: 10.3389/fphar.2026.1930236

Correction: Harpagophytum procumbens in musculoskeletal disorders: current evidence and comparison with NSAIDs

Jin Young Hong 1,, Junseon Lee 1,, Hyunseong Kim 1, Hyun Kim 1, Wan-Jin Jeon 1, Changhwan Yeo 1, Yoon Jae Lee 1, Ho-Yeon Go 2, In-Hyuk Ha 1,*
PMCID: PMC13458184  PMID: 42582659

There was a mistake in Scheme 1 and Figure 1 as published. The images for Scheme 1 and Figure 1 were inadvertently interchanged during the publication process; the image displayed as Scheme 1 should be Figure 1, and the image displayed as Figure 1 should be Scheme 1.

SCHEME 1.

Flowchart illustrating the systematic review article selection process: 319 records were identified, 60 duplicates removed, 259 screened, 100 excluded for specific reasons, 159 assessed for eligibility, 52 review articles excluded, and 113 articles included in the review, with an additional 6 review articles included for supplementary data.

Overview of the literature search, screening, categorization, and narrative synthesis process used in this structured narrative review of Harpagophytum procumbens and NSAIDs.

FIGURE 1.

Schematic comparison of the anti-inflammatory mechanisms of Harpagophytum procumbens and nonsteroidal anti-inflammatory drugs (NSAIDs) following external inflammatory stimuli. The diagram illustrates that Harpagophytum procumbens modulates multiple intracellular signaling pathways, including NF-κB, MAPKs, COX-2, and 5-LOX, leading to reduced production of pro-inflammatory cytokines, inflammatory mediators, and inflammatory gene expression. In contrast, NSAIDs primarily inhibit cyclooxygenase (COX), thereby reducing prostaglandin E2 (PGE2) synthesis and suppressing inflammation through this mechanism. The two cell schematics visually compare the broader multi-target actions of Harpagophytum procumbens with the more selective mechanism of NSAIDs.

Schematic representation of the anti-inflammatory mechanisms of HP compared to NSAIDs. HP exerts anti-inflammatory effects through multiple pathways, including inhibition of MAPKs and NF-κB signaling, activation of PPAR-γ, and suppression of pro-inflammatory mediators (e.g., cytokines, COX-2, 5-LOX, cPLA2). In contrast, NSAIDs act mainly by inhibiting COX-2 and reducing PGE2 synthesis.

The corrected Scheme 1 and Figure 1 appear below.

The original version of this article has been updated.

Footnotes

Edited and reviewed by: Albino Martins, Universidade do Minho Instituto de Investigacao em Biomateriais Biodegradaveis e Biomimeticos, Portugal

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