Ferroptosis is a newly discovered form of regulated cell death dependent on iron and reactive oxygen species (ROS). It directly or indirectly affects the activity of glutathione peroxidases (GPXs) under the induction of small molecules, causing membrane lipid peroxidation due to redox imbalances and excessive ROS accumulation, damaging the integrity of cell membranes. Ferroptosis is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes, and the accumulation of lipid peroxidation. Myocardial ischemia‐reperfusion injury (MIRI) is an unavoidable risk event for acute myocardial infarction. Ferroptosis is closely associated with MIRI, and this relationship is discussed in detail here. This review systematically summarizes the process of ferroptosis and the latest research progress on the role of ferroptosis in MIRI to provide new ideas for the prevention and treatment of MIRI.

Salvia miltiorrhiza is widely used traditional Chinese medicine in the treatment of diabetes kidney disease (DKD). Tanshinone IIA (Tan IIA) are one of the main components of the root of red-rooted Salvia miltiorrhiza Bunge. However, whether Tan IIA delay the progression of DKD and the underlying mechanisms are unknown. Clarify the mechanisms underlying the occurrence and progression of DKDs from a novel viewpoint and confirm the function and mechanism of Tan IIA. We experimented with models of DKD (db/db mice) and cultured human renal glomerular endothelial cells (HRGECs). We measured the biochemical indicators of mouse blood and urine to confirmed that Tan IIA exerted protective effects on the kidneys of db/db mice. Renal histopathology and immunohistochemical staining were used to determine the role of Tan IIA. High glucose-induced HRGECs pyroptosis based on the results of western blot, CCK-8 cell viability test, calcein/PI staining, ROS/superoxide anion generation and transmission electron microscope. We also confirmed that Tan IIA alleviated HRGEC pyroptosis through the same methods. The relationships between oxidative induction and regulation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation were investigated using western blot following the application of an NLRP3 inhibitor and oxidative stress inhibitor. Tan IIA alleviated kidney injury and improved the levels of urine, blood indicators, the expression of NLRP3 and thioredoxin-interacting protein (Txnip) in db/db mice kidney. In vitro, high glucose inhibited HRGECs viability, increased ROS generation, enhanced the proportion of propidium iodide-stained cells. In addition, we discovered the expression of GSDMD-NT, NLRP3, cleaved IL-1β, cleaved caspase-1, and Txnip increased, but the expression of Trx1 decreased after treated by high glucose. These changes were partially ameliorated by Tan IIA. Hyperglycemia could induce pyroptosis in renal glomerular endothelial cells. However, Tan IIA could delay the progression of DKD by inhibiting pyroptosis by regulating the Txnip/NLRP3 inflammasome.

Pulmonary fibrosis is a progressively aggravating lethal disease that is a serious public health concern. Although the incidence of this disease is increasing, there is a lack of effective therapies. In recent years, the pathogenesis of pulmonary fibrosis has become a research hotspot. p53 is a tumor suppressor gene with crucial roles in cell cycle, apoptosis, tumorigenesis, and malignant transformation. Previous studies on p53 have predominantly focused on its role in neoplastic disease. Following in-depth investigation, several studies have linked it to pulmonary fibrosis. This review covers the association between p53 and pulmonary fibrosis, with the aim of providing novel ideas to improve the clinical diagnosis, treatment, and prognosis of pulmonary fibrosis.

Pyroptosis is a pattern of programmed cell death that significantly differs from apoptosis and autophagy in terms of cell morphology and function. The process of pyroptosis is characterized predominantly by the formation of gasdermin protein family‐mediated membrane perforation, cell collapse, and the release of inflammatory factors, including IL‐1β and IL‐18. In recent years, with the rise of pyroptosis research, scholars have devoted time to study the mechanism of pyroptosis in kidney‐related diseases. Pyroptosis is probably involved in kidney diseases through two pathways: the caspase‐1‐mediated canonical pathway and the caspase‐4/5/11‐mediated noncanonical pathway. In addition, some scholars have identified targets for the treatment of kidney‐related diseases from the viewpoint of pyroptosis and developed corresponding medicines, which may become a recommendation for prognosis, targeted treatment, and clinical diagnosis of kidney diseases. This paper focuses on the up‐to‐date advances in the field of pyroptosis, especially on the key pathogenic role of pyroptosis in the development and progression of kidney diseases. It presents a more in‐depth understanding of the pathogenesis of kidney diseases and introduces novel therapeutic targets for the prevention and clinical treatment of kidney diseases.

6‐Gingerol (6‐G) is known to alleviate myocardial ischemia/reperfusion injury. However, the underlying molecular mechanisms of 6‐G myocardial protection are not known. In this study, the protective effect of 6‐G on ischemia/reperfusion (I/R) damage and whether such a mechanism was related to apoptosis inhibition and activation of phosphoinositide 3‐kinases (PI3K)/serine/threonine kinase (Akt) signaling pathway were investigated. Rats were subjected to I/R in the presence or absence of 6‐G and the changes of cardiac function, infarct size and histopathological changes, and the levels of cardiac troponin T, creatine kinase‐MB, and myocardial apoptosis were examined. The expression of caspase‐3, PI3K, p‐Akt, and Akt was also determined. We found that 6‐G (6 mg/kg) pretreatment significantly improved heart function and ameliorated infarct size and histopathological changes and cardiac troponin T and creatine kinase‐MB levels induced by I/R. Moreover, pretreatment with 6‐G significantly inhibited myocardial apoptosis and caspase‐3 activation induced by I/R. 6‐G also upregulated expression of PI3K, p‐Akt, and Akt in myocardial tissues. Taken together, these findings suggest that 6‐G inhibits apoptosis and activates PI3K/Akt signaling in response to myocardial I/R injury as a possible mechanism to attenuate I/R‐induced injury in heart. These results might be important for developing novel strategies for preventing myocardial I/R injury.