{"doi":"10.3389/fphys.2023.1270554","title":"Editorial: Inflammation and oxidative stress in vascular and renal disease: role of the inflammasome and pyroptosis","abstract":"Cardiovascular diseases are the leading cause of death worldwide, causing more than 17.9 million deaths in 2019, according to the World Health Organization. In particular, vascular and renal diseases, including hypertension, atherosclerosis, diabetic nephropathy, and chronic kidney disease, pose significant health challenges worldwide. Although inflammation and oxidative stress are critical and common factors in the development and progression of these conditions, we are far from having a complete understanding of the molecular mechanisms involved. This lack of understanding of how inflammation and oxidative stress contribute to vascular and renal pathology hinders the development of effective therapies for the treatment of the affected patients. This article collection highlights the implication of different novel pathways, from molecular mechanisms of inflammasome activation to monocyte-derived extracellular vesicles, sex-dependent pathways, and new biomarkers of oxidative stress in these diseases. Here, we briefly introduce and review the highlights of each article's contribution in the following section.In this article collection, Ertuglu et al. authored a comprehensive review of the current literature regarding the role of inflammation and oxidative stress in salt-sensitive hypertension (1), emphasizing the role of NLRP3 inflammasome activation and discussing potential therapeutic approaches to this disease. This review paper offers valuable insights into this emerging area of research, providing updated evidence on genetic polymorphisms in NLRP3 as well as IL-1β genes associated with hypertension in humans while also reviewing evidence of activation of the inflammasome in animal models of salt-sensitive hypertension. The authors also review the NLRP3 inflammasome's implication in the development of vascular dysfunction during hypertension, as well as recent evidence that suggests that oxidative stress triggers the activation of this inflammasome. Moreover, this review also highlights the proinflammatory effect of isolevuglandins (IsoLGs), lipid-derived protein modifications that have been recently associated with increased sodium reabsorption in the kidney and have an important role on T cell activation (1).The first original paper in this collection covers the topic of sex differences in the mechanisms involved in blood pressure regulation. Using the spontaneously hypertensive rat (SHR), a wellestablished animal model of essential hypertension, Sullivan et al. investigated the intriguing hypothesis that differences in apoptosis drive the decreased blood pressure and kidney inflammatory response that is common in female SHRs (2). After using a pan-caspase inhibitor to decrease apoptosis in both sexes, the authors observed similar decreases in renal apoptosis in male and female rats, but no alterations in the blood pressure or renal T cell profiles. Therefore, they concluded that sex differences in apoptosis do not contribute to sex differences in blood pressure or renal T cell infiltration during essential hypertension.In the second original paper, Pitzer Mutchler and colleagues studied the implications of Mg 2+ deficiency in the pathogenesis of hypertension. In particular, the authors investigated the interplay between Mg 2+ deficiency, NLRP3 inflammasome activation in monocytes and dendritic cells, and the production of IsoLGs by these cells. As mentioned above, IsoLGs are thought to play a critical role in activating the inflammatory cascade during hypertension. By using a combination of in vivo and in vitro approaches, the authors demonstrate that depletion of dietary Mg 2+ results in increased blood pressure levels, as well as exaggerated activation of the NLRP3 inflammasome and IL-1β production (3). These findings may have important clinical implications since commonly used medications like diuretics lead to a deficiency of Mg 2+ . Preeclampsia, or new onset hypertension developed after the 20 th week of gestation,","journal":"Frontiers in Physiology","year":2023,"id":411144,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9608,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":326880,"name":"Rodrigo O. Marañón","orcid":"0000-0002-3743-7420","position":1,"is_corresponding":false},{"id":372078,"name":"Santiago Cuevas","orcid":"0000-0002-0832-5446","position":2,"is_corresponding":false},{"id":485176,"name":"Carmen De Miguel","orcid":"0000-0002-2323-3670","position":0,"is_corresponding":true}],"reference_count":1,"raw_metadata":null,"created_at":"2026-07-19T01:21:38.940853Z","pmid":"37736489","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}