Pro-inflammatory cytokines may induce late preconditioning in unstable angina patients.
Late preconditioning can be induced by a wide variety of stimulus, including non-pharmacological and pharmacological. Thus, late preconditioning is a universal response of the heart to stress and it requires the simultaneous activation of multiple stress-responsive genes. Recently, compelling evidence has evolved that the up-regulation of pro-inflammatory cytokines plays an important role in induction of the late phase of ischemic preconditioning in rodent models. However, the role of cytokines in induction of late preconditioning in humans has not been explored. Patients with unstable coronary syndromes have a systemic inflammatory responses with increase of the pro-inflammatory cytokines, such as TNFalpha, IL-6. And some researchers find the patients undergoing CABG with unstable angina have a better cardioprotective effect caused by late preconditioning characterized by the activated NF-kappaB and synthesized effector proteins (HSP72 and eNOS). Therefore, we hypothesize that pro-inflammatory cytokines may induce late preconditioning in unstable angina patients directly or through remote preconditioning. It is difficult to test our hypotheses in vivo, but in vitro, human tissue culture with isolated atrial myocardium could be tested. If the hypotheses is true, the biological complication is immense. A new physiological function of pro-inflammatory cytokines is found, that is, inducing endogenous cytoprotection. From the clinical point of view, administering the appropriate pro-inflammatory cytokines will be beneficial to patients before cardiac surgery.
Wang
Yong-Yi
YY
Department of Cardiovascular Surgery, The Second XiangYa Hospital, Central South University, Middle Renmin Road No. 139, Changsha, Hunan 410011, People's Republic of China.
Yin
Bang-Liang
BL
D000789:Angina, Unstable / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D016207:Cytokines / Q000097:blood / Q000502:physiology*; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D053582:Interleukin-1alpha / Q000097:blood / Q000502:physiology / Q000627:therapeutic use; D015850:Interleukin-6 / Q000097:blood / Q000502:physiology / Q000627:therapeutic use; D019194:Ischemic Preconditioning / Q000379:methods*; D051381:Rats; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000502:physiology / Q000627:therapeutic use
D016207:Cytokines; D053582:Interleukin-1alpha; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha