인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Post-COVID syndrome (PCS) affects approximately 3-17% of individuals following acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and poses a potential global health burden. While improved assessment strategies are emerging, mechanistic insights and treatment options remain limited. This study investigates molecular mechanisms underlying PCS using single-cell RNA (scRNA) transcriptomics combined with in vitro validation. scRNA analysis is performed on nasal biopsies from 25 patients with moderate or severe PCS to investigate differential cell types, signalling pathways, and cell-cell communication. Air-liquid interface cultures are used to validate findings, focusing on the TNFα-TGFβ axis. Severe PCS shows reduced numbers of ciliated cells, increased immune cell infiltration, and heightened inflammatory signaling that drives TGFβ and TNFα upregulation, in the absence of a detectable viral load. These changes trigger epithelial-mesenchymal transition, basal cell expansion and a mis-stratified nasal epithelium. In vitro experiments confirm TGFβ and TNFα as causal cytokines promoting ciliated cell loss and increased basal cell abundance. These findings indicate a sustained severe PCS is not driven by ongoing viral load but by immune cell activity and chronic cytokine production. Targeting the TNFα-TGFβ axis may mitigate immune-mediated nasal tissue damage and support epithelium restoration, offering a potential therapeutic strategy for PCS.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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