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Abstract Currently, global warming, invasive alien species and tourism development pose major threats to Natural World Heritage sites, and the strengthening of conservation methods and management programs in buffer zones is urgent for the sustainable development of sites. Agroforestry, as a nature-based solution, not only promotes the buffer zone to effectively maintain the Outstanding Universal Value of the heritage site, but also balances the relationship between the conservation of the heritage site and the economic development of the buffer zone, and effectively enhances the protection of the buffer zone in response to various threats. However, there is currently a lack of comprehensive understanding of research trends, research focuses, and recent developments, regarding the conservation of natural heritage sites and buffer zone agroforestry development. Therefore, this study utilized the Scopus database along with Excel and Bibliometrix software to conduct a bibliometric analysis and explore and visualize popular research topics and foreword issues related to Natural World Heritage conservation and buffer zone agroforestry development. We discuss the current publication trends and quantity, keyword and abstract word frequencies, thematic maps and evolutions, journal productivity, national publication outputs, collaboration relationships, and contributing institutions. The research shows that the relationship between biodiversity conservation and agroforestry has been the focus of research in the field since 1992, and the development of agroforestry has contributed to biodiversity conservation in heritage sites. However, there have been fewer studies addressing the geomorphic and aesthetic value of agroforestry conservation, and little attention has been paid to buffer zone development. Based on this, this manuscript suggests that in the future, emphasis should be placed on the linkage between the development of buffer zones and heritage conservation, especially in the Karst World Heritage Sites with ecologically fragile, and that the role of agroforestry development in buffer zones should be strengthened in the promotion of ecological balance and sustainable development of the sites, to provide scientific references for the conservation and development of other geoheritage sites around the globe.

Acute myocardial infarction (AMI) is the leading cause of death worldwide. Identifying the pathways that block cardiac cell death is a therapeutic strategy for ischemic heart disease. We found that long noncoding RNA (lncRNA) myocardial infarction-regulatory factor (MIRF) promoted ischemic myocardial injury by regulating autophagy through targeting miR-26a. However, the role of MIRF-miR-26a in apoptosis during AMI has not been delineated. In this study, we found the downregulation of miR-26a both in the heart of myocardial infarction (MI) mice and in H2O2-treated cardiomyocytes. miR-26a silencing resulted in apoptosis, whereas overexpression of miR-26a attenuated H2O2-induced apoptosis through promoting mitochondrial ATP content and increasing mitochondrial membrane potential (MMP). Moreover, forced expression of miR-26a protected against MI-induced cardiac injury and attenuated cardiac apoptosis. Further studies showed that miR-26a inhibited apoptosis through regulation of Bak1. Furthermore, MIRF decreased ATP content and MMP through regulating miR-26a, which then promoted the cardiomyocyte apoptosis. In contrast, deficiency of MIRF promoted mitochondrial ATP content and increased MMP, and then inhibited MI or H2O2-induced cardiac apoptosis, which was abolished by miR-26a inhibitor. Taken together, these results suggested that MIRF contributed to cardiomyocyte apoptosis through modulating Bak1 by regulation of miR-26a, which can be a potential therapeutic target for the treatment of ischemic heart disease.

Lung disease: managing misbehaving mitochondria The hormone melatonin could protect lung cells from the damage associated with respiratory diseases such as pulmonary fibrosis. Several studies have linked such damage with abnormal activity of the mitochondria, with these essential metabolic organelles churning out damaging ‘reactive oxygen species’ (ROS), compounds that induce premature cell aging and death. Melatonin can mitigate ROS production, and researchers led by Haihai Liang at China’s Harbin Medical University have demonstrated that it can prevent injury to airway epithelial cells in a mouse model of lung disease. Melatonin treatment countered much of the damage, resulting in significantly longer survival, and the team identified a target molecule in the mitochondria that may be responsible for this effect. This approach could offer hope for a family of diseases with a poor prognosis and limited treatment options.