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A series of Co1−xZnxFe2O4 particulate nano-ferrites with x = 0, 0.2, 0.4, 0.5, 0.6, 0.7, and 0.8, fabricated by the co-precipitation method, have been investigated. The lattice parameter is found to increase and particle size decreases with increasing x. Mössbauer spectroscopy at room temperature exhibits ferromagnetic hyperfine splitting sextet peaks with a doublet peak overlapping at its center as Zn contents x < 0.6, and only a single doublet as x ≥ 0.7. The fitting results of Mössbauer spectra reveal the occupation rule of nonmagnetic Zn2+ ions and superparamagnetic behavior. At room temperature, the superparamagnetic excitation plays an important role in the magnetic properties. The fitted hyperfine magnetic field of the octahedral and tetrahedral sublattices decreases with increasing Zn content. The saturation magnetization and coercivity monotonously reduce to a small value. However, at low temperature of 5 K, the saturation magnetization (Ms) fully reflects the occupation of Zn ions. Zn substitutions that occupied first the tetrahedral sites cause the increase of magnetization when Zn content is below 0.4, while when Zn content is above 0.4, Zn substitutions occupied both the tetrahedral sites and the octahedral site, which leads to the decrease of magnetization.

Phenotypic plasticity of vascular smooth muscle cells (VSMCs) under stress is believed to be a key factor in neointima formation. Lactate dehydrogenase A (LDHA), a key enzyme for glycolysis, has been demonstrated to promote the proliferation and migration of VSMCs. However, the mechanism by which LDHA regulates this process is still unclear. Here we show that the crotonylation and mono-ubiquitination of LDHA are increased in platelet-derived growth factor (PDGF)-BB-induced proliferative VSMCs. Crotonylation at lysine 5 (K5) activates LDHA through tetramer formation to enhance lactate production and VSMCs growth. Mono-ubiquitination at K76 induces the translocation of LDHA into mitochondria, which promotes mitochondria fission and subsequent the formation of lamellipodia and podosomes, thereby enhancing VSMC migration and growth. Furthermore, the increase of crotonylation and ubiquitination were also observed in the carotid arteries of ligation injury mice. Deletion of LDHA K5 crotonylation or K76 mono-ubiquitination decreases ligation-induced neointima formation. Our study reveals a novel mechanism that combines VSMC metabolic reprogramming and behavioral abnormity through crosstalk between LDHA K5 crotonylation and K76 mono-ubiquitination.