The balance of inflammation is critical to the repair of spinal cord injury (SCI), which is one of the most devastating traumas in human beings. Inflammatory cytokines, the direct mediators of local inflammation, have differential influences on the repair of the injured spinal cord. Some inflammatory cytokines are demonstrated beneficial to spinal cord repair in SCI models, while some detrimental. Various animal researches have revealed that local delivery of therapeutic agents efficiently regulates inflammatory cytokines and promotes repair from SCI. Quite a few clinical studies have also shown the promotion of repair from SCI through regulation of inflammatory cytokines. However, local delivery of a single agent affects only a part of the inflammatory cytokines that need to be regulated. Meanwhile, different individuals have differential profiles of inflammatory cytokines. Therefore, future studies may aim to develop personalized strategies of locally delivered therapeutic agent cocktails for effective and precise regulation of inflammation, and substantial functional recovery from SCI.

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Fine particulate matter ≤2.5 μm (PM2.5) air pollution is regarded as one of the prominent risk factors that contributes to morbidity and mortality globally, among which cardiovascular disease (CVD) has been strongly associated with PM2.5 exposure and is a leading cause of death. Atherosclerosis (AS), the common pathological basis of many CVDs, is a progressive syndrome characterized by the accumulation of lipids and fibrous plaque in the arteries. Recent epidemiological and toxicological studies suggest that PM2.5 may also contribute to the development of AS, even at levels below the current air quality standards. In this paper, the complete pathological process of atherosclerotic plaque from occurrence to rupture leading to CVD was elaborated. Then, the growing epidemiological evidence linking PM2.5 to AS in humans was reviewed and summarized. Furthermore, the potential mechanisms of PM2.5‐mediated AS were discussed, including oxidative stress, inflammation, endothelial dysfunction, abnormal lipid metabolism, disturbance of the autonomic nervous system, and abnormal coagulation function. This paper aimed to provide a comprehensive view of the effect of PM2.5 on the occurrence and development of AS for better prevention and mitigation of adverse health impacts due to PM2.5 air pollution.

It is a common clinical phenomenon that blood infiltrates into the injured tendon caused by sports injuries, accidental injuries, and surgery. However, the role of blood infiltration into the injured tendon has not been investigated. We established a rat model in which the injured Achilles tendon was infiltrated with autologous whole blood and confirmed that blood caused acute inflammation in the short term and more severe heterotopic ossification (HO) in the long term. Then we found that blood treatment increased cell apoptosis and decreased cell adhesion and tenogenic gene expression of TSPCs. Furthermore, Blood treatment promoted osteochondrogenic differentiation of TSPCs. Next, we used RNA-seq to find that the PI3K/AKT signaling pathway was activated in blood-treated tendon tissues. By inhibiting PI3K with a small molecule drug LY294002, the expression of osteochondrogenic genes was markedly downregulated while the expression of tenogenic genes was significantly upregulated. Our findings indicate that the upregulated PI3K/AKT signaling pathway is implicated in the aggravation of tendon HO. Therefore, inhibitors targeting the PI3K/AKT pathway would be a promising approach to treat blood-induced tendon HO.