Public Health Measures to Address the Impact of Climate Change on Population Health-Proceedings from a Stakeholder Workshop.

BACKGROUND: The World Health Organization identified climate change as the 21st century's biggest health threat. This study aimed to identify the current knowledge base, evidence gaps, and implications for climate action and health policymaking to address the health impact of climate change, including in the most underserved groups. METHODS: The Horizon-funded project ENBEL ('Enhancing Belmont Research Action to support EU policy making on climate change and health') organised a workshop at the 2021-European Public Health conference. Following presentations of mitigation and adaptation strategies, seven international researchers and public health experts participated in a panel discussion linking climate change and health. Two researchers transcribed and thematically analysed the panel discussion recording. RESULTS: Four themes were identified: (1) 'Evidence is key' in leading the climate debate, (2) the need for 'messaging about health for policymaking and behaviour change' including health co-benefits of climate action, (3) existing 'inequalities between and within countries', and (4) 'insufficient resources and funding' to implement national health adaptation plans and facilitate evidence generation and climate action, particularly in vulnerable populations. CONCLUSION: More capacity is needed to monitor health effects and inequities, evaluate adaptation and mitigation interventions, address current under-representations of low- or middle-income countries, and translate research into effective policymaking.

N-myristoyltransferase deficiency impairs activation of kinase AMPK and promotes synovial tissue inflammation.

N-myristoyltransferase (NMT) attaches the fatty acid myristate to the N-terminal glycine of proteins to sort them into soluble and membrane-bound fractions. Function of the energy-sensing AMP-activated protein kinase, AMPK, is myristoylation dependent. In rheumatoid arthritis (RA), pathogenic T cells shift glucose away from adenosine tri-phosphate production toward synthetic and proliferative programs, promoting proliferation, cytokine production, and tissue invasion. We found that RA T cells had a defect in NMT1 function, which prevented AMPK activation and enabled unopposed mTORC1 signaling. Lack of the myristate lipid tail disrupted the lysosomal translocation and activation of AMPK. Instead, myristoylation-incompetent RA T cells hyperactivated the mTORC1 pathway and differentiated into pro-inflammatory TH1 and TH17 helper T cells. In vivo, NMT1 loss caused robust synovial tissue inflammation, whereas forced NMT1 overexpression rescued AMPK activation and suppressed synovitis. Thus, NMT1 has tissue-protective functions by facilitating lysosomal recruitment of AMPK and dampening mTORC1 signaling.