Research map: Dipeptidyl peptidase 3-mediated iNOS activation participates in myocardial injury in sepsis partially through reduction of angiotensin-(1-7)

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  1. Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase · John D. MacMicking · 1995 · 1452 citations · Cited by this paper
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  16. Common biomarkers associated with brown adipose tissue in type 2 diabetes and metabolic dysfunction-associated fatty liver disease: a bioinformatics analysis and mouse model investigations experiments · 2026 · Related
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  21. Inhibition of circulating dipeptidyl-peptidase 3 restores cardiac function in a sepsis-induced model in rats: A proof of concept study · Benjamin Deniau · 2020 · 79 citations · Cited by this paper
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  23. SELECTIVE INDUCIBLE NITRIC OXIDE SYNTHASE INHIBITION DURING LONG-TERM HYPERDYNAMIC PORCINE BACTEREMIA · Martin Matějovič · 2004 · 74 citations · Cited by this paper
  24. Myocardial oxidative stress correlates with left ventricular dysfunction on strain echocardiography in a rodent model of sepsis · Bereketeab Haileselassie · 2017 · 60 citations · Cited by this paper
  25. Promotion of vascular integrity in sepsis through modulation of bioactive adrenomedullin and dipeptidyl peptidase 3 · Dirk P. T. van Lier · 2020 · 53 citations · Cited by this paper
  26. A double-blind, placebo-controlled, randomised, multicentre, proof-of-concept and dose-finding phase II clinical trial to investigate the safety, tolerability and efficacy of adrecizumab in patients with septic shock and elevated adrenomedullin concentration (AdrenOSS-2) · Christopher Geven · 2019 · 49 citations · Cited by this paper
  27. Identification of dipeptidyl peptidase 3 as the Angiotensin-(1–7) degrading peptidase in human HK-2 renal epithelial cells · Nildris Cruz‐Diaz · 2016 · 45 citations · Cited by this paper
  28. Circulating Dipeptidyl Peptidase 3 Modulates Systemic and Renal Hemodynamics Through Cleavage of Angiotensin Peptides · Adrien Picod · 2024 · 40 citations · Cited by this paper
  29. Inhibition of circulating dipeptidyl-peptidase 3 by procizumab in experimental septic shock reduces catecholamine exposure and myocardial injury · Bruno Garcia · 2024 · 37 citations · Cited by this paper
  30. The phosphoinositide‐3 kinase signaling is involved in neuroinflammation in hypertensive rats · Xing Lin Tan · 2017 · 36 citations · Cited by this paper
  31. Angiotensin 1–7 in an experimental septic shock model · Bruno Garcia · 2023 · 35 citations · Cited by this paper
  32. Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats · Hsin-Jung Tsai · 2021 · 34 citations · Cited by this paper
  33. Dipeptidyl peptidase 3, a marker of the antagonist pathway of the renin–angiotensin–aldosterone system in patients with heart failure · Eva M. Boorsma · 2021 · 22 citations · Cited by this paper
  34. ACE2 alleviates sepsis-induced cardiomyopathy through inhibiting M1 macrophage via NF-κB/STAT1 signals · Xue Xiao · 2024 · 21 citations · Cited by this paper
  35. Alterations in the renin-angiotensin system during septic shock · Camille Benaroua · 2025 · 21 citations · Cited by this paper
  36. DPP3: From biomarker to therapeutic target of cardiovascular diseases · Peng Ye · 2022 · 20 citations · Cited by this paper
  37. Long noncoding RNA MCM3AP-AS1 attenuates sepsis-induced cardiomyopathy by improving inflammation, oxidative stress, and mitochondrial function through mediating the miR-501-3p/CADM1/STAT3 axis · Xiangbi Nie · 2024 · 20 citations · Cited by this paper
  38. The impact of cardiac dysfunction on acute respiratory distress syndrome and mortality in mechanically ventilated patients with severe sepsis and septic shock: An observational study · Brian M. Fuller · 2014 · 19 citations · Cited by this paper
  39. Angiotensin 1–7 mitigates rhabdomyolysis induced renal injury in rats via modulation of TLR-4/NF-kB/iNOS and Nrf-2/heme‑oxygenase-1 signaling pathways · Elshymaa A. Abdel‐Hakeem · 2022 · 18 citations · Cited by this paper

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