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Bacterial extracellular vesicles (BEVs) released by Gram-negative bacteria modulate host cell functions by delivering bacterial components to host cells. Endothelial dysfunction\u00a0is an\u00a0important\u00a0early\u00a0event\u00a0in the pathogenesis of hypertension, yet the impact of\n                      <jats:italic>K.pn<\/jats:italic>\n                      -secreted EVs (\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs) on endothelial function remains unclear. This study aimed to investigate the effects of\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs on endothelial function and to elucidate the underlying mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs were purified from the bacterial suspension using ultracentrifugation and characterized by transmission electron microscopy nanoparticle tracking analysis, and EV marker expression. Endothelium-dependent relaxation was measured using a\u00a0wire myograph after in vivo or ex vivo treatment with\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs. Superoxide anion production was measured by confocal microscopy and HUVEC senescence was assessed by SA-\u03b2-gal activity. SIRT1 overexpression or activator was utilized to investigate the underlying mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our data showed that\n                      <jats:italic>K.pn<\/jats:italic>\n                      significantly impaired acetylcholine-induced endothelium-dependent relaxation and increased superoxide anion production in endothelial cells in vivo. Similarly, in vivo and ex vivo studies showed that\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs caused significant endothelial dysfunction, endothelial provocation, and increased blood pressure. Further examination revealed that\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs reduced the levels of SIRT1 and p-eNOS and increased the levels of NOX2, COX-2, ET-1, and p53 in endothelial cells. Notably, overexpression or activation of SIRT1 attenuated the adverse effects and protein changes induced by\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs on endothelial cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      This study reveals a novel role of\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs in endothelial dysfunction and dissects the relevant mechanism involved in this process, which will help to establish a comprehensive understanding of\n                      <jats:italic>K.pn<\/jats:italic>\n                      EVs in endothelial dysfunction and hypertension from a new scope.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12964-024-02002-0","type":"journal-article","created":{"date-parts":[[2025,1,12]],"date-time":"2025-01-12T20:42:41Z","timestamp":1736714561000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1"],"prefix":"10.1186","volume":"23","author":[{"given":"Xinxin","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinghua","family":"Cui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zanbo","family":"Ding","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziyan","family":"Tian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yiming","family":"Kong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linghai","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xueying","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Han","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengshuo","family":"Cui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinwei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huina","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,1,13]]},"reference":[{"issue":"1","key":"2002_CR1","doi-asserted-by":"publisher","first-page":"135","DOI":"10.1038\/s41392-022-00974-4","volume":"7","author":"K Hou","year":"2022","unstructured":"Hou K, Wu Z-X, Chen X-Y, Wang J-Q, Zhang D, Xiao C, Zhu D, Koya JB, Wei L, Li J, et al. 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