In a review article (mechanistic overview on mitochondrial regulation by natural products) Qin et al. from the Qingdao Medical College & Qingdao University, Pharmaceutical University, Nanjing published in the Neural Regeneration Research journal to summarize how natural products modulate mitochondrial dysfunction (biogenesis, dynamics, transport, mitophagy, apoptosis, oxidative stress) for stroke treatment, and identify barriers to clinical translation. Natural products act via multi-target mechanisms on mitochondrial processes to exert neuroprotection in both ischemic and hemorrhagic stroke models, but clinical translation is impeded by product complexity, lack of standardization, insufficient multicenter data, and unclear long-term safety. Future directions include advanced technologies (single-cell sequencing, organoid models) and multicenter trials 1).
*✅ Strengths*
*❌ Weaknesses*
Score: 7/10 – Strong mechanistic organization and translational awareness, but limited methodological critique and insufficient attention to pharmacokinetics and evidence quality.
Natural compounds show multi-faceted neuroprotection via mitochondrial modulation in animal/stem cell stroke models. However, they are not yet ready for clinical use due to regulatory, safety, and reproducibility gaps. Neurosurgeons should await human data before considering these agents.
A well-structured mechanistic review that identifies promising mitochondrial-targeting natural products, but lacks rigorous evaluation of experimental quality and clinical feasibility—future translational efforts are needed.