Table 2 Characteristics and main findings of relevant studies reporting on myocardial, kidney, and lung injury
From: Protective effects of dexmedetomidine in vital organ injury: crucial roles of autophagy
Study/ref. | Experimental model | Types of injury | DEX administration | Status of autophagy | Associated genes or pathways | Main findings |
|---|---|---|---|---|---|---|
Myocardial injury | ||||||
Yu et al. 2019 [28] | Rat | Septic myocardial dysfunction | Injection, 50 μg/kg | Promoted | Upregulating 7nAChR and the PI3K/Akt pathway | DEX attenuates the myocardium injury by mediating autophagic flux; DEX decreases the myocardium apoptosis and inflammatory response mediated by increased autophagy by activating α7nAChR and the PI3K/Akt pathway |
Zhang et al. 2020 [54] | Rat | Myocardial ischemia/reperfusion injury | Intravenous injection, 10 μg/kg | Inhibited | Upregulating the SIRT1/mTOR pathway | DEX reduces cardiomyocyte apoptosis, oxidative stress, and inflammatory reactions via upregulating the SIRT1/mTOR axis and decreasing overautophagy in myocardial ischemia/reperfusion injury rats |
Xiao et al. 2021 [55] | Cardiomyocytes | Myocardial ischemia/reperfusion injury | 5 μM DEX was added to the culture media | Upregulated | Upregulating AMP-activated protein kinase (AMPK) and phospho AMPK | DEX protected human cardiomyocytes from apoptosis and was associated with autophagy; the protection of DEX for H/R injury was AMPK dependent and α2-adrenergic receptor dependent |
Li et al. 2021 [41] | Rat | Myocardial ischemia/reperfusion injury | Injected through the jugular vein catheter, 10 μg/kg | Inhibited | Upregulating Beclin1 and activating the PI3K/Akt pathway | DEX upregulates the phosphorylation of Beclin 1 at S295 site by activating the PI3K/Akt pathway and reduces the interactions of Atg14L–Beclin1–Vps34 complex, thus inhibiting autophagy and protecting against myocardial ischemia/reperfusion injury |
Kidney injury | ||||||
Lempiainen et al. 2014 [29] | Rat | Cerebral kidney ischemia–reperfusion injury | Intravenous injection, 10 μg/kg | Enhanced | Upregulating renal p38 MAPK | DEX preconditioning ameliorates kidney ischemia–reperfusion injury and inflammatory response via the enhancement of autophagy and the regulation of the p38-CD44 pathway |
Yang et al. 2020 [56] | Rat | Lipopolysaccharide-induced acute kidney injury | Intraperitoneally, 30 μg/kg | Enhanced | Upregulating the expression of p-AMPK and downregulating p-mTOR | DEX ameliorates inflammatory response by reducing NLRP3 inflammasome and inflammatory cytokines by enhancing autophagy via the AMPK/mTOR pathway |
Zhao et al. 2020 [57] | Rat | Lipopolysaccharide-induced acute kidney injury | Intraperitoneally, 30 μg/kg | Enhanced | Inhibition of the PI3K/AKT/mTOR pathway | DEX protects against LPS-induced acute kidney injury by enhancing autophagy, thus removing the damaged mitochondria and reducing oxidative stress and apoptosis through the α2-AR and inhibition of the PI3K/AKT/mTOR pathway |
Lung injury | ||||||
Zhang et al. 2017 [30] | Rat | Lung ischemia/reperfusion injury | Administered intravenously, 10 μg/kg | Inhibited | Upregulating the level of HIF‑1α, downregulating BNIP3, BNIP3 L, and LC3II | Preconditioning with DEX provided protection against lung injury in a dose-dependent manner by inhibiting autophagy, which might be associated with the upregulation of HIF-1α and downregulation of BNIP3 and BNIP3 L |
Ding et al. 2018 [58] | Mouse | Lipopolysaccharide-induced acute lung injury | Intravenously injected, 50 μg/kg | Inhibited | Inhibition of the TLR4-NF-κB pathway | DEX protects against acute lung injury via reducing the inflammatory response and inhibiting autophagy-related proteins and signaling pathway |
Li et al. 2021 [59] | Rat | Toxic shock-induced lung injury | Intraperitoneally, 50 μg/kg | Inhibited | Decreasing the expression of pERK1/2 protein | DEX protects against lung injury by inhibiting autophagy and inflammation |