ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
CD38
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Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13citing papers in PubMed
–field-weighted citation impact
What it found
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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.
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Who cites it
13 citing papers in PubMed.
- scH16S-Seq Maps Klebsiella pneumoniae-Associated Myeloid States and Reveals a CD38-NAD Immunometabolic Axis That Impairs Lysosomal Acidification in Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Acute Kidney Injury-to-Chronic Kidney Disease Transition-Associated Macrophage Subtypes: Biological Functions and Intercellular Crosstalk.International journal of molecular sciences · 2026Review
- CD38-activated macrophages drive age-related placental senescence by depleting NADNature communications · 2026Article
- The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.Seminars in immunopathology · 2026Review
- Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.Science advances · 2026Article
- Circulating CD38 shows stronger association with incident heart failure in women despite lower levels: sex differences and kidney-function context.Biology of sex differences · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- TRAP5 Inhibition Targeting Scar-Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Targeting Itga8 Mitigates Neurogenic Bladder Fibrosis Driven by Trem2⁺ Macrophage-Derived Fn1 via FAK/RhoA/ROCK Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Sema3dInternational journal of biological sciences · 2026Article
- Mechanisms of Macrophage Glycolytic Reprogramming and Interventional Effects of Traditional Chinese Medicine on Renal Fibrosis.International journal of general medicine · 2026Review
- Article
Corrections and comments
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Authors and funding
11 authors.
Weijian YaoRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Menghan LiuRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Zehua LiRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Lei QuRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Shuang SuiRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Chengang XiangRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Lei JiangRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Suxia WangLaboratory of Electron Microscopy Pathological Center, Peking University First Hospital, Beijing 100034, P.R. China.
Gang LiuRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China.
Ying ChenRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China. Electronic address: ychen0822@126.com.
Li YangRenal Division, Peking University Institute of Nephrology, Key Laboratory of Renal Disease-Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University)-Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases-Chinese Academy of Medical Sciences, Beijing Key Laboratory of Precision Medicine and New-drug/Equipment Development for Severe Kidney Disease, Peking University First Hospital, Beijing 100034, P.R. China. Electronic address: li.yang@bjmu.edu.cn.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) encompasses a spectrum of conditions, varying from mild and self-limiting to severe cases that can lead to chronic kidney disease (CKD). Macrophages are crucial in the progression from AKI to CKD, yet the diversity of macrophage subsets complicates the identification of key functional types. We established a detailed single-cell atlas of mononuclear macrophages from the onset of AKI through its progression to CKD. Our results indicate that a macrophage subset with high CD38 expression is closely linked to renal fibrosis following AKI in both mouse model and AKI patients. These CD38
Indexed as
Acute Kidney InjuryADP-ribosyl Cyclase 1MacrophagesMembrane GlycoproteinsNADAnimalsDisease Models, AnimalFibrosisHumansMaleMiceMice, Inbred C57BLRenal Insufficiency, ChronicADP-ribosyl Cyclase 1Cd38 protein, mouseMembrane GlycoproteinsNADacute kidney injuryCD38hi macrophagesNAD+renal fibrosisscRNA sequencingsenescence
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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.