GRP78 effectively protect hypoxia/reperfusion-induced myocardial apoptosis via promotion of the Nrf2/HO-1 signaling pathway.

Myocardial infarction is a major cause of death worldwide. Despite our understanding of the pathophysiology of myocardial infarction and the therapeutic options for treatment have improved substantially, acute myocardial infarction remains a leading cause of morbidity and mortality. Recent findings revealed that GRP78 could protect myocardial cells against ischemia reperfusion injury-induced apoptosis, but the exact function and molecular mechanism remains unclear.

Involvement of microRNA-23b-5p in the promotion of cardiac hypertrophy and dysfunction via the HMGB2 signaling pathway.

The processes involved in the progression of myocardial cells towards hypertrophy and its gradual transition to heart failure represent a multifactorial health disorder. The aim of this study was to identify the molecular mechanism(s) underlying the abnormal overexpression of miR-23b-5p and its involvement in the promotion of cardiac hypertrophy and dysfunction via HMGB2. A type 9 recombinant adeno-associated virus (rAAV9) was employed to manipulate miR-23b-5p expression under conditions of thoracic aortic constriction (TAC)-/angiotensin-II (Ang-II)-induced cardiac dysfunction.

Edaravone Improves Septic Cardiac Function by Inducing an HIF-1/HO-1 Pathway.

Septic myocardial dysfunction remains prevalent and raises mortality rate in patients with sepsis. During sepsis, tissues undergo tremendous oxidative stress which contributes critically to organ dysfunction. Edaravone, a potent radical scavenger, has been proved beneficial in ischemic injuries involving hypoxia-inducible factor- (HIF-) 1, a key regulator of a prominent antioxidative protein heme oxygenase- (HO-) 1.

PPAR- Activation Prevents Septic Cardiac Dysfunction via Inhibition of Apoptosis and Necroptosis.

Sepsis-induced cardiac dysfunction remains one of the major causes of death in intensive care units. Overwhelmed inflammatory response and unrestrained cell death play critical roles in sepsis-induced cardiac dysfunction. Peroxisome proliferator-activated receptor- (PPAR-) has been proven to be cardioprotective in sepsis.

Brain-Derived Neurotrophic Factor Attenuates Septic Myocardial Dysfunction via eNOS/NO Pathway in Rats.

Sepsis-induced myocardial dysfunction increases mortality in sepsis, yet the underlying mechanism is unclear. Brain-derived neurotrophic factor (BDNF) has been found to enhance cardiomyocyte function, but whether BDNF has a beneficial effect against septic myocardial dysfunction is unknown. Septic shock was induced by cecal ligation and puncture (CLP).

[Limb remote ischemic preconditioning attenuates liver ischemia reperfusion injury by activating autophagy via modulating PPAR-γ pathway].

Objective: To investigate the effect of limb remote ischemic preconditioning (RIPC) on hepatic ischemia/reperfusion (IR) injury and the underlying mechanisms.


Methods: Rats were subjected to partial hepatic IR (60 min ischemia followed by 24 hours reperfusion) with or without RIPC, which was achieved by 3 cycles of 10 min-occlusion and 10 min-
reperfusion at the bilateral femoral arteries interval 30 min before ischemia. Some rats were treated with a new PPAR-γ inhibitor, T0070907, before RIPC.

Sevoflurane pretreatment attenuates TNF-α-induced human endothelial cell dysfunction through activating eNOS/NO pathway.

Endothelial dysfunction induced by oxidative stress and inflammation plays a critical role in the pathogenesis of cardiovascular diseases. The anesthetic sevoflurane confers cytoprotective effects through its anti-inflammatory properties in various pathologies such as systemic inflammatory response syndrome and ischemic-reperfusion injury but mechanism is unclear. We hypothesized that sevoflurane can protect against tumor necrosis factor (TNF)-α-induced endothelial dysfunction through promoting the production of endothelium-dependent nitric oxide (NO).

[Silencing of MST1 expression by siRNA diminishes TNF-α- mediated human umbilical vein endothelial cell apoptosis].

Objective: To elucidate the effects of mammalian sterile 20-like kinase 1 (MST1) gene on tumor necrosis factor (TNF)-α-mediated human umbilical vein endothelial cell (HUVEC) apoptosis.

Methods: Cultured HUVECs were treated with either vehicle or TNF-α (1-100 ng/mL) for 24 hours. Cell apoptosis was measured by TUNEL staining, and MST1 activity was analyzed by Western blot.

Effects of down-regulation of microRNA-23a on TNF-α-induced endothelial cell apoptosis through caspase-dependent pathways.

Aims: Endothelial cell injury induced by inflammatory factors plays a critical role in the pathogenesis of numerous vascular diseases. MicroRNAs are well known to be implicated in cell proliferation and apoptosis in inflammatory responses; however, it remains to be determined whether microRNAs are associated with tumour necrosis factor (TNF)-α-mediated endothelial cell injury. The aim of the present study was to investigate the role of microRNAs in TNF-α-induced endothelial cell apoptosis.