MiRNA-Mediated Mechanisms of Cardiac Protection in Ischemic and Remote Ischemic Preconditioning-A Qualitative Systematic Review.

Background: Ischemic preconditioning (IPC) and remote ischemic preconditioning (RIPC) protect myocardial tissue against subsequent ischemia and reperfusion injury (IRI) and have a high potential to improve patient outcome. The mediators and mechanisms of protection through IPC and RIPC remain largely unknown, but micro-RNAs (miRNAs) are promising candidates.

Methods: Systematic review of Medline and Embase databases for biomedical scientific literature.

Aberrant plasma IL-7 and soluble IL-7 receptor levels indicate impaired T-cell response to IL-7 in human tuberculosis.

T-cell proliferation and generation of protective memory during chronic infections depend on Interleukin-7 (IL-7) availability and receptivity. Regulation of IL-7 receptor (IL-7R) expression and signalling are key for IL-7-modulated T-cell functions. Aberrant expression of soluble (s) and membrane-associated (m) IL-7R molecules is associated with development of autoimmunity and immune failure in acquired immune deficiency syndrome (AIDS) patients.

Are microRNAs suitable biomarkers of immunity to tuberculosis?

Background: MicroRNAs (miRNAs) are crucial regulators of human immunity e.g. against Mycobacterium tuberculosis.

Effects of remote ischemic preconditioning and myocardial ischemia on microRNA-1 expression in the rat heart in vivo.

Remote ischemic preconditioning (RIPC) is an easily applicable method for protecting the heart against a subsequent ischemia and reperfusion (I/R) injury. However, the exact molecular mechanisms underlying RIPC are unknown. We examined the involvement of microRNAs (miRNAs) and in particular the expression of miRNA-1 (miR-1) in RIPC and myocardial ischemia.

Decreased expression of miR-21, miR-26a, miR-29a, and miR-142-3p in CD4⁺ T cells and peripheral blood from tuberculosis patients.

The vast majority of Mycobacterium tuberculosis (M. tuberculosis) infected individuals are protected from developing tuberculosis and T cells are centrally involved in this process. MicroRNAs (miRNA) regulate T-cell functions and are biomarker candidates of disease susceptibility and treatment efficacy in M.