AIM
A systematic review was conducted to clarify the association between long-term prenatal systemic glucocorticoid use of at least 7 days and offspring neurodevelopmental and neuropsychiatric outcomes.
METHODS
PubMed, Embase, Web of Science, the Cumulative Index to Nursing and Allied Health Literature, Cochrane Library and PsycINFO were searched from inception to March 8, 2026. We identified four observational studies that evaluated prenatal systemic glucocorticoid exposure and offspring neurodevelopmental outcomes, including autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and intellectual disability (ID). Study quality was assessed, and a narrative synthesis was performed.
RESULTS
Three nationwide cohorts (covering more than 1.2 million pregnancies) reported significantly elevated risks of ASD and ADHD following prenatal glucocorticoid exposure (adjusted risk ratio 1.3-1.5). The association with ID was inconsistent and non-significant (risk ratio 1.1-1.4). A single-centre study of 74 subjects did not find any significant cognitive differences.
CONCLUSION
Prenatal glucocorticoid use was associated with modestly increased risks of ASD and ADHD. However, residual confounding by maternal disease severity remained a major limitation and a specific medication-related effect could not be conclusively established. Glucocorticoid use should focus on the lowest dose and shortest duration, with clear counselling. Further research is required.
TRIAL REGISTRATION
International Prospective Register of Systematic Reviews: CRD420261327850.
Guang-Nan Mei, Jin Gan, Ya-Fang Xia et al.· Acta paediatrica· 0 citations
BACKGROUND AND PURPOSE
The molecular mechanisms underlying denervation-induced muscle atrophy remain incompletely understood, and effective therapeutic interventions are currently lacking. Tectorigenin (TG), a natural isoflavonoid, has demonstrated antioxidant and metabolic regulatory activities. This study investigated whether TG also alleviates denervation-induced muscle atrophy via activation of the AMPK/SIRT1/PGC-1α signalling pathway.
EXPERIMENTAL APPROACH
A sciatic nerve transection model was established in ICR mice to evaluate the therapeutic effects of TG. Histomorphology, oxidative stress markers, mitochondrial function and pathway activity were assessed. A nutrient deprivation-induced C2C12 myotube atrophy model was used for in vitro validation. Pathway-specific inhibitors (Compound C, EX-527 and SR18292) were applied both in vivo and in vitro to confirm mechanistic involvement.
KEY RESULTS
TG treatment significantly improved muscle wet weight ratio, myofibre cross-sectional area and myosin heavy chain expression in denervated mice. It reduced levels of atrophy-related ubiquitin ligases, attenuated oxidative stress and improved mitochondrial integrity. TG reversed the denervation-induced suppression of AMPK/SIRT1/PGC-1α signalling and downstream effectors. In C2C12 myotubes, TG dose-dependently ameliorated atrophy and up-regulated SIRT1/PGC-1α. Pharmacological inhibition of AMPK, SIRT1 or PGC-1α abolished TG's protective effects, both in vitro and in vivo.
CONCLUSIONS AND IMPLICATIONS
TG mitigates denervation-induced muscle atrophy through a multi-mechanistic approach involving activation of the AMPK/SIRT1/PGC-1α axis, enhancement of mitochondrial dynamics and restoration of redox homeostasis. This study identifies TG as a promising candidate for clinical translation in the treatment of neurogenic muscle atrophy.
Boya Liu, Fei Xue, Xingxing Fang et al.· British Journal of Pharmacol...· 0 citations
This review systematically elaborates on the key pathological roles and molecular mechanisms of ERS and the triggered UPR in Parkinson's disease and discusses various intervention approaches, their research progress, and associated challenges.
Xin Chen, Zihao Zhao, Xinlei Yao et al.· Biochemical Pharmacology· 6 citations
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