A growing body of research suggests that authoritarian regimes are responsive to societal actors, but our understanding of the sources of authoritarian responsiveness remains limited because of the challenges of measurement and causal identification. By conducting an online field experiment among 2,103 Chinese counties, we examine factors that affect officials' incentives to respond to citizens in an authoritarian context. At baseline, we find that approximately one‐third of county governments respond to citizen demands expressed online. Threats of collective action and threats of tattling to upper levels of government cause county governments to be considerably more responsive, whereas identifying as loyal, long‐standing members of the Chinese Communist Party does not increase responsiveness. Moreover, we find that threats of collective action make local officials more publicly responsive. Together, these results demonstrate that top‐down mechanisms of oversight as well as bottom‐up societal pressures are possible sources of authoritarian responsiveness.

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We develop a theory of how an authoritarian regime interactively uses information manipulation, such as propaganda or censorship, and policy improvement to maintain social stability. The government can depict the status quo policy more popularly supported than it actually is, while at the same time please citizens directly by enacting a costly reform. We show that the government’s ability of making policy concessions reduces its incentive to manipulate information and improves its credibility. Anticipating a higher chance of policy concessions and less information manipulation, citizens are more likely to believe the government-provided information and support the regime. Our model provides an explanation for the puzzling fact that reform coexists with selective information disclosure in authoritarian countries like China.

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There is growing evidence that microRNAs are implicated in pulmonary arterial hypertension (PAH), but underlying mechanisms remain elusive. Here, we identified that miR-223 was significantly downregulated in chronically hypoxic mouse and rat lungs, as well as in pulmonary artery and pulmonary artery smooth muscle cells (PASMC) exposed to hypoxia. Knockdown of miR-223 increased PASMC proliferation. In contrast, miR-223 overexpression abrogated cell proliferation, migration and stress fiber formation. Administering miR-223 agomir in vivo antagonized hypoxia-induced increase in pulmonary artery pressure and distal arteriole muscularization. RhoB, which was increased by hypoxia, was identified as one of the targets of miR-223. Overexpressed miR-223 suppressed RhoB and inhibited the consequent phosphorylation of myosin phosphatase target subunit (MYPT1) and the expression of myosin light chain of myosin II (MLC2), which was identified as another target of miR-223. Furthermore, serum miR-223 levels were decreased in female patients with PAH associated with congenital heart disease. Our study provides the first evidence that miR-223 can regulate PASMC proliferation, migration, and actomyosin reorganization through its novel targets, RhoB and MLC2, resulting in vascular remodeling and the development of PAH. It also highlights miR-223 as a potential circulating biomarker and a small molecule drug for diagnosis and treatment of PAH.