Author

Yushi Hu

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Review Open access Aug 2026

The role of ECM-PIEZO1-axis-mediated mechanosensation in the central nervous system

Central nervous system (CNS) diseases are characterized by high rates of disability and mortality, and their pathological progression is generally accompanied by abnormal remodeling of the extracellular matrix (ECM) composition and mechanical properties. The mechanosensitive cation channel PIEZO1 is widely expressed in neurons, microglia, astrocytes, oligodendrocytes, and endothelial cells of the CNS. It can precisely sense mechanical signals such as ECM stiffness, viscoelasticity, shear stress, and matrix protein cross-linking, and convert them into intracellular calcium signals and downstream biochemical reactions, thereby mediating the mechanobiological crosstalk between the ECM and cells and playing a key role in physiological processes such as neurodevelopment, synaptic plasticity, blood–brain barrier (BBB) homeostasis, neuroimmune regulation, and cell fate determination. In diseases such as Alzheimer’s disease (AD), ischemic stroke (IS), and multiple sclerosis (MS), abnormal stiffening or remodeling of the ECM can lead to excessive activation of PIEZO1, which, by regulating pathways such as nuclear factor-kappa B (NF-κB), Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ), calcium/calmodulin-dependent protein kinase II (CaMKII), and glutathione peroxidase 4 (GPX4), exacerbates neuroinflammation, BBB disruption, myelin destruction, neuronal ferroptosis, and defective axonal regeneration. This article systematically reviews the cellular expression profile of PIEZO1 in the CNS, the ECM-mediated activation mechanisms, and downstream signaling networks. It elucidates the regulatory role of the ECM-PIEZO1 axis in both the physiological functions and typical diseases of the CNS, aiming to provide a theoretical basis and new insights for mechanobiological research into the mechanisms and targeted therapies of CNS diseases.

Xiping Zhang, Yu-Chen Zhu, Si-Qi Song et al. · Frontiers in Neurology · 0 citations

Jul 2026

Quinoa regulates hepatic lipid metabolism in MASLD mice via PPARγ-PLIN2.

Metabolic dysfunction-associated steatotic liver disease (MASLD) primarily results from excessive nutrient consumption, with lifestyle modifications, particularly dietary interventions, constituting a principal strategy for its management. This study sought to examine the ameliorative effects of a quinoa diet (QD) on hepatic lipid metabolism in mice with MASLD. Six-week-old male C57BL/6J mice were fed with a QD for 12 weeks, and age-matched male mice were subjected to a high-fat diet (HFD) to establish obese MASLD models, followed by QD intervention. Compared with the chow diet (CD) group, QD supplementation maintained lower levels of Lee's index, serum AST and ALT, confirming its regulatory effect on hepatic fat accumulation. In MASLD mice, QD supplementation markedly decreased Lee's index, blood glucose, ALT, AST, LDL-C, TC and TG contents. It also downregulated the gene expression of ACC, FAS and SCD-1 as well as the protein levels of PPARγ and PLIN2, thereby alleviating HFD-triggered hepatic lipid metabolism disorders. Lipids and lipid-like molecules were the most significantly altered metabolites in QD-treated mice, accounting for 50.87% of all differential metabolites. Collectively, quinoa demonstrates the capacity to enhance hepatic lipid metabolism in mice with metabolic-associated steatotic liver disease (MASLD), with the PPARγ-PLIN2 signaling pathway potentially serving as a central therapeutic target. These findings indicate that quinoa holds significant promise as a functional food for the intervention and mitigation of MASLD.

Peijie Liu, Jingyang Wan, Luping Qiao et al. · Food & Function · 0 citations