Pyroptosis is a relatively newly discovered programmed cell death accompanied by an inflammatory response. In the classical view, pyroptosis is mediated by caspases-1,-4,-5,-11 and executed by GSDMD, however, recently it was demonstrated that caspase-3 and-8 also participate in the process of pyroptosis, by cleaving GSDMD/E and GSDMD respectively. Different from autophagy and apoptosis, many pores are formed on the cell membrane during pyroptosis, which makes the cell membrane lose its integrity, eventually leading to the release of cytokines interleukin(IL)-1β and IL-18. When the body is infected with pathogens or exposed to some stimulations, pyroptosis could play an immune defense role. It is found that pyroptosis exists widely in infectious and inflammatory respiratory diseases such as acute lung injury, bronchial dysplasia, chronic obstructive pulmonary disease, and asthma. Excessive pyroptosis may accompany airway inflammation, tissue injury, and airway damage, and induce an inflammatory reaction, leading to more serious damage and poor prognosis of respiratory diseases. This review summarizes the relationship between pyroptosis and related respiratory diseases.

OBJECTIVE: Gasdermin D (GSDMD) is a cytoplasmic protein that is encoded by the gasdermin family GSDMD gene and is the ultimate executor of pyroptosis. Pyroptosis is a mode of lysis and inflammation that regulates cell death, ultimately leading to cell swelling and rupture. In sepsis, a dysregulated host response to infection frequently results in hyperinflammatory responses and immunosuppression, eventually leading to multiple organ dysfunction. Pyroptosis regulates innate immune defenses and plays an important role in the process of inflammatory cell death, and the absence of any link in the entire pathway from GSDMD to pyroptosis causes bacterial clearance to be hampered. Under normal conditions, the process of pyroptosis occurs much faster than apoptosis, and the threat to the body is also much greater.
METHODS: We conducted a systematic review of relevant reviews and experimental articles using the keywords sepsis, Gasdermin D, and Pyroptosis in the PubMed, Scopus, Google Scholar, and Web of Science databases.
CONCLUSIONS: Combined with the pathogenesis of sepsis, it is not difficult to find that pyroptosis plays a key role in bacterial inflammation and sepsis. Therefore, GSDMD inhibitors may be used as targeted drugs to treat sepsis by reducing the occurrence of pyroptosis. This review mainly discusses the key role of GSDMD in sepsis.

BACKGROUND: Chronic kidney disease-mineral and bone disorders (CKD-MBD) have been associated with poor health outcomes, including diminished quality and length of life. Standard management for CKD-MBD includes phosphate-restricted diet, active vitamin D, vitamin D analogs, and phosphate binders. Persistently elevated parathyroid hormone (PTH) levels may require the addition of Cinacalcet hydrochloride (cinacalcet) which sensitizes calcium receptors on the parathyroid glands. The objective of this systematic review is to compare the effect of cinacalcet versus standard treatment in patients with CKD-MBD.
METHODS: Data sources will include MEDLINE, EMBASE, the Cochrane Register of Controlled Trials, and Web of Science from 1996 to June 2015. Teams of two reviewers will, independently and in duplicate, screen titles and abstracts and potentially eligible full text reports to determine eligibility, and subsequently abstract data and assess risk of bias in eligible trials. We will calculate the effect estimates (risk ratios or mean differences) and 95 % confidence intervals, as well as statistical measures of variability in results across studies using random effect models for patient-important and intermediate outcomes. We will use the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) approach to rate the quality of evidence about estimates of effect on an outcome-by-outcome basis. We will present our results with a GRADE summary table.
CONCLUSIONS: Our review will explore the effect of cinacalcet versus standard treatment in patients with CKD-MBD. The results of this systematic review will help guide management of this patient population, and identify targets for future research.
BACKGROUND: PROSPERO CRD42015020318 http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42015020318.

BACKGROUND: Cardiovascular events are the leading cause of death in end stage renal disease (ESRD). Adherence to phosphate binding medication plays a vital role in reducing serum phosphorus and associated cardiovascular risk. This poses a challenge for patients as the regimen is often complex and there may be no noticeable impact of adherence on symptoms. There is a need to establish the level of nonadherence to phosphate binding medication in renal dialysis patients and identify the factors associated with it.
METHODS: The online databases PsycINFO, Medline, Embase and CINAHL were searched for quantitative studies exploring predictors of nonadherence to phosphate binding medication in ESRD. Rates and predictors of nonadherence were extracted from the papers.
RESULTS: Thirty four studies met the inclusion criteria. There was wide variation in reported rates of non-adherence (22-74% patients nonadherent, mean 51%). This can be partially attributed to differences in the way adherence has been defined and measured. Demographic and clinical predictors of nonadherence were most frequently assessed but only younger age was consistently associated with nonadherence. In contrast psychosocial variables (e.g. patients\' beliefs about medication, social support, personality characteristics) were less frequently assessed but were more likely to be associated with nonadherence.
CONCLUSIONS: Nonadherence to phosphate binding medication appears to be prevalent in ESRD. Several potentially modifiable psychosocial factors were identified as predictors of nonadherence. There is a need for further, high-quality research to explore these factors in more detail, with the aim of informing the design of an intervention to facilitate adherence.