Sepsis is an abnormal condition with multiple organ dysfunctions caused by the uncontrolled infection response and one of the major diseases that seriously hang over global human health. Besides, sepsis is characterized by high morbidity and mortality, especially in intensive care unit (ICU). Among the numerous subsequent organ injuries of sepsis, myocardial injury is one of the most common complications and the main cause of death in septic patients. To better manage septic inpatients, it is necessary to understand the specific mechanisms of sepsis induced myocardial injury (SIMI). Therefore, this review will elucidate the pathophysiology of SIMI from the following certain mechanisms: apoptosis, mitochondrial damage, autophagy, excessive inflammatory response, oxidative stress and pyroptosis, and outline current therapeutic strategies and potential approaches in SIMI.

Sepsis is a clinical syndrome characterized by a dysregulated host response to infection, leading to life-threatening organ dysfunction. It is a high-fatality condition associated with a complex interplay of immune and inflammatory responses that can cause severe harm to vital organs. Sepsis-induced myocardial injury (SIMI), as a severe complication of sepsis, significantly affects the prognosis of septic patients and shortens their survival time. For the sake of better administrating hospitalized patients with sepsis, it is necessary to understand the specific mechanisms of SIMI. To date, multiple studies have shown that programmed cell death (PCD) may play an essential role in myocardial injury in sepsis, offering new strategies and insights for the therapeutic aspects of SIMI. This review aims to elucidate the role of cardiomyocyte’s programmed death in the pathophysiological mechanisms of SIMI, with a particular focus on the classical pathways, key molecules, and signaling transduction of PCD. It will explore the role of the cross-interaction between different patterns of PCD in SIMI, providing a new theoretical basis for multi-target treatments for SIMI.

Aims: This study aimed to evaluate the effects of VC on SIMI in rats. Methods: In this study, the survival rate of high dose VC for SIMI was evaluated within 7 days. Rats were randomly assigned to three groups: Sham group, CLP group, and high dose VC (500 mg/kg i.v.) group. The animals in each group were treated with drugs for 1 day, 3 days or 5 days, respectively. Echocardiography, myocardial enzymes and HE were used to detect cardiac function. IL-1β, IL-6, IL-10 and TNF-α) in serum were measured using ELISA kits. Western blot was used to detect proteins related to apoptosis, inflammation, autophagy, MAPK, NF-κB and PI3K/Akt/mTOR signaling pathways. Results: High dose VC improved the survival rate of SIMI within 7 days. Echocardiography, HE staining and myocardial enzymes showed that high-dose VC relieved SIMI in rats in a time-dependent manner. And compared with CLP group, high-dose VC decreased the expressions of pro-apoptotic proteins, while increased the expression of anti-apoptotic protein. And compared with CLP group, high dose VC decreased phosphorylation levels of Erk1/2, P38, JNK, NF-κB and IKK α/β in SIMI rats. High dose VC increased the expression of the protein Beclin-1 and LC3-II/LC3-I ratio, whereas decreased the expression of P62 in SIMI rats. Finally, high dose VC attenuated phosphorylation of PI3K, AKT and mTOR compared with the CLP group. Significance: Our results showed that high dose VC has a good protective effect on SIMI after continuous treatment, which may be mediated by inhibiting apoptosis and inflammatory, and promoting autophagy through regulating MAPK, NF-κB and PI3K/AKT/mTOR pathway.

Translationally controlled tumor protein (TCTP), also known as histamine-releasing factor (HRF) or fortilin, is a highly conserved protein found in various species. To date, multiple studies have demonstrated the crucial role of TCTP in a wide range of cellular pathophysiological processes, including cell proliferation and survival, cell cycle regulation, cell death, as well as cell migration and movement, all of which are major pathogenic mechanisms of tumorigenesis and development. This review aims to provide an in-depth analysis of the functional role of TCTP in tumor initiation and progression, with a particular focus on cell proliferation, cell death, and cell migration. It will highlight the expression and pathological implications of TCTP in various tumor types, summarizing the current prevailing therapeutic strategies that target TCTP.

This study aims to explore the mechanism by which the Translationally controlled tumor protein (TCTP) promotes hyperplasia of the mammary glands (HMG). In this study, the TCTP (Tpt1^flox/flox) and TCTP (Tpt1^KI/KI) gene mice were respectively mated with MMTV-Cre to obtain mice withmammary glands-specific TCTP knockout (TCTP ^cKO) and overexpression (TCTP ^KI). Prepare the HMG animal model by using estrogen combined with progesterone. After the establishment of the TCTP ^cKO and TCTP ^KI mouse models, they are uniformly referred to as HMG ^cKO and HMG ^KI. Hematoxylin and Eosin (H&E) staining and hormone and receptor expression levels were detected. Detect the levels of TCTP, P53, p-AKT, as well as the indicators related to cell apoptosis and cell cycle in the breast tissues of each group. The H&E results showed that compared with the HMG group, the ductal cavity dilation and the number of milk glands in the breast tissue of the HMG ^cKO group were significantly reduced, while the HMG ^KI group exhibited obvious mammary gland hyperplasia. The results showed that compared with the HMG group, the expression levels of Ki67, E₂, FSH, LH, ERα, PR, TCTP, p-AKT, p-BAD, Bcl-2, Cyclin D1, CDK4 and CDK6 in the mammary tissues of the HMG ^cKO group were significantly decreased, while the expression levels of PROG, ERβ, P53, Bax and P27 were significantly increased. In the HMG ^KI group, the opposite results were observed. In our research, it was confirmed that TCTP inhibits cell apoptosis and promotes cell cycle progression by regulating the AKT/P53 signaling pathway, leading to abnormal hyperplasia of the mammary glands. In HMG, by regulating the expression level of TCTP, the effect of treating HMG can be achieved.