The Journal of Clinical Investigation
Journal
The Journal of Clinical Investigation is a premier venue for discoveries in basic and clinical biomedical science that will advance the practice of medicine. Source
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| Scope | National |
|---|---|
| Language | English |
| Country | United States of America |
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| Frequency | Monthly |
| Accepts contributed content | Yes |
Recent Articles
Search ArticlesGoing to the source: pancreatic lymph nodes maintain stem-like CD8 + T cells in human type 1 diabetes
Abstract Where does autoimmune persistence reside in type 1 diabetes (T1D)? Detailed investigation of the pancreas and pancreatic lymph nodes (PLNs) may provide more definitive answers, yet most studies in these target tissues have been confined to mouse models. In nonobese diabetic (NOD) mice, disease development is prevented by PLN ablation, and these LNs harbor a stem-like population of autoreactive CD8+ T cells. In this issue, Peters et al.
Reverse genetics in humanized mice reveals CARD8-mediated pyroptosis causing pancytopenia in human DPP9 deficiency
Abstract Loss-of-function mutation in the human gene dipeptidyl peptidase 9 (DPP9) causes Hatipoglu syndrome leading to severe inflammasomopathy. A key feature of the disease is pancytopenia, and patients require bone marrow transplantation, but the mechanism of cell loss is unclear, since Dpp9-mutant mice have normal hematopoiesis, suggesting that a distinct mechanism of disease occurs in humans.
UA-30 ameliorates motor deficits through RalA-mediated mitophagy in ALS mice
Research ArticleCell biologyNeuroscience Open Access | 10.1172/JCI202787 Authorship note: BZ, YH, and TS contributed equally to this work. Published in Volume 136, Issue 18 on September 15, 2026 J Clin Invest. 2026;136(18):e202787. https://doi.org/10.1172/JCI202787. © 2026 Zhang et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Ferroptosis as a target mechanism in heart and kidney disease
Conclusions and future directions Ferroptosis has rapidly emerged as a central mechanism linking lipid peroxidation and cellular redox homeostasis to diverse pathological states, ranging from degenerative disorders to cancer. Considerable progress has been made in defining its biochemical hallmarks, including the essential roles of GPX4, System Xc–, FSP1, and ACSL4, as well as the broader metabolic networks that regulate susceptibility.
Imaging B cell maturation antigen in multiple myeloma
Commentary Open Access | 10.1172/JCI210178 Published in Volume 136, Issue 18 on September 15, 2026 J Clin Invest. 2026;136(18):e210178. https://doi.org/10.1172/JCI210178. © 2026 Song et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Corrigendum to A midbrain–cortical circuit mediated by a claustrum neuronal ensemble orchestrates drug-paired context memory processing
Original citation: J Clin Invest. 2026;136(5):e196944. https://doi.org/10.1172/JCI196944 Citation for this corrigendum: J Clin Invest. 2026;136(18):e211416. https://doi.org/10.1172/JCI211416 After publication of this article, the authors became aware of data entry errors for Supplemental Figure 2H. Specifically, five of the raw values for the Saline‑CNO (n = 6) group were incorrect and were identical to raw values for the METH‑CNO (n = 6) group.
Hemiplegic migraine: genetics and pathophysiology
Abstract Rare monogenic subtypes of migraine with aura, which include an autosomal dominant form of hemiplegic migraine (HM), are caused by exonic mutations whose functional consequences can be studied in cellular and animal models of the disease. This allows investigation of the neurobiological mechanisms at the molecular, cellular, and circuit level. Here, I review current knowledge of the genetics and pathophysiology of HM.
Corrigendum to E3 ubiquitin ligase Listerin regulates macrophage cholesterol efflux and atherosclerosis by targeting ABCA1
Original citation: J Clin Invest. 2025;135(16):e186509. https://doi.org/10.1172/JCI186509 Citation for this corrigendum: J Clin Invest. 2026;136(18):e211585.
Corrigendum to Genome-wide CRISPR screen identifies a cytokine-enhancer circuit driving HIF-2α activation in renal cancer
Corrigendum Open Access | 10.1172/JCI211482 Published in Volume 136, Issue 18 on September 15, 2026 J Clin Invest. 2026;136(18):e211482. https://doi.org/10.1172/JCI211482. © 2026 Fang et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. View PDF Jun Fang, Jeremy M.
Evidence for a tubular basement membrane–cilia connection in autosomal dominant polycystic kidney disease pathogenesis
Commentary Open Access | 10.1172/JCI210031 Published in Volume 136, Issue 18 on September 15, 2026 J Clin Invest. 2026;136(18):e210031. https://doi.org/10.1172/JCI210031. © 2026 Sussman, et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.