Temozolomide (TMZ) is the first-line chemotherapy drug that has been used to treat glioma for over a decade, but the benefits are limited by half of the treated patients who acquired resistance. Studies have shown that glioma TMZ resistance is a complex process with multiple factors, which has not been fully elucidated. Ferroptosis, which is a new type of cell death discovered in recent years, has been reported to play an important role in tumor drug resistance. The present study reviews the relationship between ferroptosis and glioma TMZ resistance, and highlights the role of ferroptosis in glioma TMZ resistance. Finally, the investigators discussed the future orientation for ferroptosis in glioma TMZ resistance, in order to promote the clinical use of ferroptosis induction in glioma treatment.

In patients with cancer, drug tolerance often occurs during the use of chemotherapy drugs, seriously affecting patient prognosis and survival. Therefore, scientists began to study the factors that affect chemotherapy drug sensitivity, and the high correlation between Schlafen-11 (SLFN11) and sensitivity to chemical drugs (mainly DNA-damaging agents, DDAs) has received increasing attention since it was discovered through bioinformatics analyses. Regarding the mechanism, SLFN11 may sensitize cells to chemotherapy drugs by preventing DNA damage repair. In recent years, SLFN11 has gradually become a hot research topic, and the results are enriching our understanding of this molecule. Indeed, the biological functions of SLFN11 under normal physiological conditions and in cancer, changes in its expression levels and mechanisms promoting apoptosis within the context of chemotherapeutic interventions have gradually been uncovered. Studies to date provide knowledge and the experimental and theoretical bases underlying SLFN11 and its effects on sensitivity to chemotherapy drugs. This review summarizes the existing research on SLFN11 with the aim of achieving a more comprehensive understanding and furthering the development of strategies to target SLFN11 in the treatment of cancer.

Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the progressive loss of memory and cognition in the aging population. However, the etiology of and therapies for AD remain far from understood. Astrocytes, the most abundant neuroglia in the brain, have recently aroused substantial concern due to their involvement in synaptotoxicity, amyloidosis, neuroinflammation, and oxidative stress. In this review, we summarize the candidate molecules of astrocytes, especially receptors and transporters, that may be involved in AD pathogenesis. These molecules include excitatory amino acid transporters (EAATs), metabotropic glutamate receptor 5 (mGluR5), the adenosine 2A receptor (A2AR), the α7-nicotinic acetylcholine receptor ( α7-nAChR), the calcium-sensing receptor (CaSR), S100β, and cannabinoid receptors. We describe the characteristics of these molecules and the neurological and pharmacological underpinnings of these molecules in AD. Among these molecules, EAATs, A2AR, and mGluR5 are strongly related to glutamate-mediated synaptotoxicity and are involved in glutamate transmission or the clearance of extrasynaptic glutamate in the AD brain. The α7-nAChR, CaSR, and mGluR5 are receptors of Aβ and can induce a plethora of toxic effects, such as the production of excess Aβ, synaptotoxicity, and NO production triggered by changes in intracellular calcium signaling. Antagonists or positive allosteric modulators of these receptors can repair cognitive ability and modify neurobiological changes. Moreover, blocking S100β or activating cannabinoid receptors reduces neuroinflammation, oxidative stress, and reactive astrogliosis. Thus, targeting these molecules might provide alternative approaches for treating AD.