Background Platelet‐to‐lymphocyte ratio (PLR) is a haematological index which reflects increased level of inflammation and thrombosis. We aimed to summarize the potential prognostic role of PLR for the in‐hospital and long‐term outcomes in ST‐segment elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention (pPCI) in a meta‐analysis. Materials and methods Relevant cohort studies were identified by search the PubMed, Cochrane's Library and Embase databases. A random‐effect model was applied to pool the results. In‐hospital and long‐term outcomes were compared between patients with higher and lower preprocedural PLR. Results Eleven cohorts with 12 619 patients were included. Pooled results showed that higher preprocedural PLR was independently associated with increased risk of in‐hospital major adverse cardiovascular events (MACE, risk ratio [RR]: 1.76, 95% confidence interval [CI]: 1.39 to 2.22, P < .001; I2 = 49%), cardiac mortality (RR: 1.91, 95% CI: 1.18 to 3.09, P = .009; I2 = 0), all‐cause mortality (RR: 2.14, 95% CI: 1.52 to 3.01, P < .001, I2 = 24%) and no reflow after pPCI (RR: 2.22, 95% CI: 1.70 to 2.90, P < .001, I2 = 59%). Moreover, higher preprocedural PLR was associated with increased risk of MACE (RR: 1.60, 95% CI: 1.25 to 2.03, I2 = 57%, P < .001) and all‐cause mortality (RR: 2.36, 95% CI: 1.53 to 3.66, I2 = 78%, P < .001) during long‐term follow‐up of up to 82 months after discharge. Conclusions Higher PLR predicts poor in‐hospital and long‐term prognosis in STEMI patients after pPCI.

Endoplasmic reticulum (ER) stress is one of the driving forces of ischemia/reperfusion (IR)-induced acute renal failure (ARF). STF-083010, an inhibitor of the endonuclease activity of inositol-requiring enzyme-1 (IRE1), has the potential to block the initiation of a prolonged unfolded protein response (UPR) that is stimulated by ER stress and alleviates the impairments due to ER stress. In the current study, it was hypothesized that STF-083010 was capable of ameliorating ER stress-related damages in IR-induced ARF. Rats were administrated with STF-083010 and were subjected to induction of ARF using a ligation method. Then the effect of STF-083010 administration on the renal structure and function, oxidative stress, and inflammation in model rats was assessed. Furthermore, the levels of expression of UPR members and downstream effectors regulating apoptosis were detected as well. The results showed that establishment of the ARF model induced ER stress and impaired the renal structure and function. Administration of STF-083010 ameliorated impairments in the structure and function of the kidneys and the effect was associated with the suppressed oxidative stress and inflammation. At the molecular level, STF-083010 inhibited the prolonged UPR by downregulating the expressions of GRP78, p-IRE1, XBP1s, CHOP, and caspase 3, partially explaining the decreased apoptotic rate. The current study evaluated the potential of STF-083010 in treating ER stress-induced symptoms in ARF for the first time, and the findings demonstrated that STF-083010 resulted in effective treatment outcomes of ARF.