ArticleThe American journal of pathology2007
Cathepsin g is required for sustained inflammation and tissue injury after reperfusion of ischemic kidneys.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- It's a Trap!-Potential of Cathepsins in NET Formation.International journal of molecular sciences · 2025Review
- Inhibition of De Novo Autoantibody Production Attenuates Chronic Antibody-Mediated Rejection of Kidney Allografts Despite Maintenance of High Donor-Specific Antibody Titers.bioRxiv : the preprint server for biology · 2025Article
- Autoantibodies against DNA topoisomerase I promote renal allograft rejection by increasing alloreactive T cell responses.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Article
- Identification of lysosome-related genes in connection with prognosis and immune cell infiltration for drug candidates in head and neck cancer.Open life sciences · 2023Article
- Single-cell analysis reveals melanocytes may promote inflammation in chronic wounds through cathepsin G.Frontiers in genetics · 2023Article
- The Potential Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Cardiovascular System, Respiratory System and Skin.International journal of molecular sciences · 2022Review
- Multi‑faceted roles of cathepsins in ischemia reperfusion injury (Review).Molecular medicine reports · 2022Review
- The Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Oral Cavity and Abdominal Organs.International journal of molecular sciences · 2022Review
- Neutrophils drive pulmonary vascular leakage in MHV-1 infection of susceptible A/J mice.Frontiers in immunology · 2022Article
- The Inhibitory Effect of Noscapine on the In Vitro Cathepsin G-Induced Collagen Expression in Equine Endometrium.Life (Basel, Switzerland) · 2021Article
- The Inhibition of Cathepsin G on Endometrial Explants With Endometrosis in the Mare.Frontiers in veterinary science · 2020Article
- Cathepsin G and Its Role in Inflammation and Autoimmune Diseases.Archives of rheumatology · 2018Review
- Increased Neutrophil Secretion Induced byFrontiers in cellular and infection microbiology · 2017Article
- Cathepsin G Is Expressed by Acute Lymphoblastic Leukemia and Is a Potential Immunotherapeutic Target.Frontiers in immunology · 2017Article
- The Multifaceted Role of the Lysosomal Protease Cathepsins in Kidney Disease.Frontiers in cell and developmental biology · 2017Review
- Identification of Neutrophil Exocytosis Inhibitors (Nexinhibs), Small Molecule Inhibitors of Neutrophil Exocytosis and Inflammation: DRUGGABILITY OF THE SMALL GTPase Rab27a.The Journal of biological chemistry · 2016Article
- Neutrophil interactions with epithelial-expressed ICAM-1 enhances intestinal mucosal wound healing.Mucosal immunology · 2016Article
- Unilateral renal ischaemia in rats induces a rapid secretion of inflammatory markers to renal lymph and increased capillary permeability.The Journal of physiology · 2016Article
- Therapeutic landscape of carfilzomib and other modulators of the ubiquitin-proteasome pathway.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Article
- Prolonged exposure to neutrophil extracellular traps can induce mitochondrial damage in macrophages and dendritic cells.SpringerPlus · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Neutrophil activation to release granules containing proteases and other enzymes is a primary cause of tissue damage during ischemia/reperfusion injury. Because the contribution of specific granule enzymes to this injury remains poorly defined, the role of cathepsin G in renal ischemia/reperfusion injury was tested. Bilateral renal ischemia led to the expiration of 64% of wild-type mice within 4 days of reperfusion, whereas all cathepsin G-deficient mice survived. Serum creatinine increased to similar levels at 24 hours after reperfusion and then decreased to background in both groups of mice. Ischemic kidneys from both groups had similar levels of neutrophil infiltration and of CXCL1, CXCL2, and myeloperoxidase protein 9 hours after reperfusion, but at 24 hours, these acute inflammatory response components were decreased more than 50% in kidneys from cathepsin G-deficient versus wild-type mice. Ischemic kidneys from surviving wild-type mice had severe tubular necrosis and tubular cell apoptosis 24 hours after reperfusion with subsequent development of fibrosis 30 days later. In contrast, ischemic kidneys from cathepsin G-deficient mice had a 70% decrease in tubular cell apoptosis with little detectable collagen deposition. These data identify cathepsin G as a critical component sustaining neutrophil-mediated acute tissue pathology and subsequent fibrosis after renal ischemia/reperfusion injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.