Acute myocardial infarction (AMI) is a life-threatening event. Even with timely treatment, acute ischemic myocardial injury and ensuing ischemia reperfusion injury (IRI) can still be difficult issues to tackle. Apart from radiological and other auxiliary examinations, laboratory tests of applicable cardiac biomarkers are also necessary for early diagnosis and close monitoring of this disorder. Heart-type fatty acid binding protein (H-FABP), which mainly exists inside cardiomyocytes, has recently emerged as a potentially promising biomarker for myocardial injury. In this review we discuss the sensitivity and specificity of H-FABP in the assessment of myocardial injury and IRI, especially in the early stage, and its long-term prognostic value in comparison with other commonly used cardiac biomarkers, including myoglobin (Mb), cardiac troponin I (cTnI), creatine kinase MB (CK-MB), C-reactive protein (CRP), glycogen phosphorylase isoenzyme BB (GPBB), and high-sensitivity cardiac troponin T (hs-cTnT). The potential and value of combined application of H-FABP with other biomarkers are also discussed. Finally, the prospect of H-FABP is summarized; several technical issues are discussed to facilitate wider application of H-FABP in clinical practice.

Background Remote ischemic preconditioning (RIPC) protects the hearts from ischemia/reperfusion (I/R) injury experimentally. In patients undergoing cardiac surgery, RIPC exhibits cardioprotection, while in studies that included diabetic patients, RIPC lost effectiveness in cardioprotection. In order to confer cardioprotection in diabetes, the threshold for RIPC has to be increased. In diabetic rats, repeated RIPC (rRIPC) for three days reduces myocardial infarction. In a recent study that included diabetic patients, rRIPC conferred beneficial effects (Balin M. et al. Cardiovasc Ther. 2019; doi: 10.1155/2019/9592378), but the mechanism is unclear. RIPC when applied well in advance of cardiac surgery conferred cardioptection that was associated increases of both cardiac STAT3 and STAT5. We hypothesized that both STAT5A and STAT5B are needed for rRIPC cardioprotection. Methods Eight‐week STZ‐induced diabetic rats received rRIPC (three episodes of 5 min occlusion of the left femoral artery followed by 5 min of reperfusion for 3 consecutive days) before being subjected to myocardial I/R (30 minutes of coronary artery ligation and 2 hours of reperfusion). In vitro, cardiac myoblast H9c2 cell hypoxia/reoxygenation (H/R) injury model was established with 6 hours of hypoxia followed by 12 hours of normoxia reoxygenation. The cells in the conditioning group were exposed to 3 cycles of 10 minutes of alternating nitrogen‐flushed hypoxia and reoxygenation as stimulated RIPC (sRIPC) 24 hours before inducing prolonged H/R. Results rRIPC reduced post‐ischemic myocardial infarct size and apoptotic cardiomyocyte death in diabetic rats (p <0.05) that was concomitant with significantly increases of myocardial p‐STAT3, p‐STAT5A, but not p‐STAT5B. In cultured H9C2 cells, sRIPC significantly attenuated the H/R‐induced increases in LDH release and the reduction in cell viability (all p<0.05, sRIPC+H/R vs. H/R). However, sRIPC mediated cellular protection was cancelled respectively by the Janus Kinase 2 Inhibitor AG490, by gene knock‐down of either STAT3 or STAT5A, but not by STAT5B gene knockdown. Conclusions Our findings suggest that STAT5A and STAT3 but not STAT5B are critical for repeated RIPC to confer cardioprotection. Support or Funding Information This study is supported by Health and Medical Research Fund (05161826) and NSFC grants(81770824 and 81670770)

Background Myocardial ischemia‐reperfusion injury is a major threat to human health, causing great cardiac morbidity and mortality worldwide. Yet, it’s even more severe among diabetic patients. Thioredoxin‐interacting protein (TXNIP), a critical regulator with its inhibitory effect against antioxidation, is a novel target during myocardial ischemia‐reperfusion injury. TXNIP is also found to be highly expressed in hyperglycemic conditions, but its role in diabetic myocardial ischemia‐reperfusion injury is unclear. The current research aimed to study the role of TXNIP in myocardial ischemia‐reperfusion injury in diabetes mellitus. Methods Diabetes was induced by streptozotocin injection via tail vein (65mg/kg) in Sprague‐Dawley rats. In vivo model of myocardial ischemia‐reperfusion injury was established as 30 minutes occlusion of the left anterior descending coronary artery and then 2 hours of reperfusion. In vitro hypoxia/re‐oxygenation (H/R) model was established as 6 hours of hypoxia and 12 hours of re‐oxygenation of H9C2 cells. Also, glucose was added to the medium at a concentration of 33 mmol/L to mimic the condition of diabetes. TXNIP small interference RNA (siRNA) was introduced to knock down the expression of TXNIP. Results The expression of TXNIP significantly increased in the diabetic rat group, together with much greater infarct size and higher release of CK‐MB after myocardial ischemia‐reperfusion injury, compared to non‐diabetic group. In vitro study showed that TXNIP expression was significantly higher in high glucose (HG) group with greater cell injury and much higher LDH release after H/R treatment, compared to normal glucose (NG) group. However, TXNIP knock‐down via siRNA could alleviate this cellular injury with lower LDH release and higher cell viability. The expression of cleaved caspase‐3 significantly decreased even after H/R treatment in the TXNIP knock‐down group. Also, down‐regulation of NF‐kB and less phosphorylation of IkBα were detected after H/R in the TXNIP knock‐down group. Further study found higher conversion of LC3II from LC3I and lower expression of p62, indicating the activation of autophagy via TXNIP knock‐down. Finally, quantitative polymerase chain reaction test revealed significantly lower gene expression of TNF‐α and IL‐6. Conclusion TXNIP is highly expressed in diabetes after myocardial ischemia‐reperfusion injury. TXNIP knock‐down can alleviate myocardial ischemia‐reperfusion injury, possibly via activating autophagy and also via inhibiting inflammation. It is reasonable to believe that TXNIP would be a potential target for the treatment of diabetic myocardial ischemia‐reperfusion injury. Support or Funding Information Supported by RGC (17118619) and NSFC (81970247)