Monolayer 2D semiconductors (e.g., MoS2) are of considerable interest for atomically thin transistors but generally limited by insufficient carrier mobility or driving current. Minimizing the lattice defects in 2D semiconductors represents a common strategy to improve their electronic properties, but has met with limited success to date. Herein, a hidden benefit of the atomic vacancies in monolayer 2D semiconductors to push their performance limit is reported. By purposely tailoring the sulfur vacancies (SVs) to an optimum density of 4.7% in monolayer MoS2, an unusual mobility enhancement is obtained and a record‐high carrier mobility (>115 cm2 V−1 s−1) is achieved, realizing monolayer MoS2 transistors with an exceptional current density (>0.60 mA µm−1) and a record‐high on/off ratio >1010, and enabling a logic inverter with an ultrahigh voltage gain >100. The systematic transport studies reveal that the counterintuitive vacancy‐enhanced transport originates from a nearest‐neighbor hopping conduction model, in which an optimum SV density is essential for maximizing the charge hopping probability. Lastly, the vacancy benefit into other monolayer 2D semiconductors is further generalized; thus, a general strategy for tailoring the charge transport properties of monolayer materials is defined.

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Background. Zinc plays a role in mitophagy and protects cardiomyocytes from ischemia/reperfusion injury. This study is aimed at investigating whether SUMOylation of Drp1 is involved in the protection of zinc ion on cardiac I/R injury. Methods. Mouse hearts were subjected to 30 minutes of regional ischemia followed by 2 hours of reperfusion (ischemia/reoxygenation (I/R)). Infarct size and apoptosis were assessed. HL-1 cells were subjected to 24 hours of hypoxia and 6 hours of reoxygenation (hypoxia/reoxygenation (H/R)). Zinc was given 5 min before reperfusion for 30 min. SENP2 overexpression plasmid (Flag-SENP2), Drp1 mutation plasmid (Myc-Drp1 4KR), and SUMO1 siRNA were transfected into HL-1 cells for 48 h before hypoxia. Effects of zinc on SUMO family members were analyzed by Western blotting. SUMOylation of Drp1, apoptosis and the collapse of mitochondrial membrane potential (ΔΨm), and mitophagy were evaluated. Results. Compared with the control, SUMO1 modification level of proteins in the H/R decreased, while this effect was reversed by zinc. In the setting of H/R, zinc attenuated myocardial apoptosis, which was reversed by SUMO1 siRNA. Similar effects were observed in SUMO1 KO mice exposed to H/R. In addition, the dynamin-related protein 1 (Drp1) is a target protein of SUMO1. The SUMOylation of Drp1 induced by zinc regulated mitophagy and contributed to the protective effect of zinc on H/R injury. Conclusions. SUMOylation of Drp1 played an essential role in zinc-induced cardio protection against I/R injury. Our findings provide a promising therapeutic approach for acute myocardial I/R injury.