JCI insightPub Date : 2026-04-09DOI: 10.1172/jci.insight.195384
Emma Specht, Lakshmi Pakanati, Meng-Ju Wu, Russell W Jenkins, Derek N Effiom, Nabeel Bardeesy, Bradley E Bernstein, Moshe Sade-Feldman, Christine G Lian, Genevieve M Boland, Elena Torlai Triglia, Sonia Cohen
{"title":"Loss of Tumor-Infiltrating Lymphocytes and Poor Response to Immunotherapy in IDH GOF Mutant Melanoma.","authors":"Emma Specht, Lakshmi Pakanati, Meng-Ju Wu, Russell W Jenkins, Derek N Effiom, Nabeel Bardeesy, Bradley E Bernstein, Moshe Sade-Feldman, Christine G Lian, Genevieve M Boland, Elena Torlai Triglia, Sonia Cohen","doi":"10.1172/jci.insight.195384","DOIUrl":"https://doi.org/10.1172/jci.insight.195384","url":null,"abstract":"<p><p>Recent innovations in melanoma treatment with immune checkpoint blockade (ICB) have improved overall outcomes for patients, however over 50% of patients still develop resistance to treatment. These patients either have intrinsic resistance, and never respond to therapy, or develop acquired resistance months or years into treatment. The mechanisms underlying ICB resistance remain poorly understood. Our data shows that isocitrate dehydrogenase gain of function (IDH GOF) mutant melanoma patients have a worse response to anti-PD1 immunotherapy. IDH mutations have been found to be oncogenic and associated with differential methylation in multiple cancers but are not yet characterized in human melanoma. Here, we investigate the clinical, immune, and transcriptional phenotypes of IDH GOF melanomas through analyses of clinical response, single-cell RNA sequencing, bulk RNA sequencing, and DNA methylation data. Single-cell data analysis shows decreased immune infiltrate and activity in the IDH GOF tumors. Bulk sequencing data demonstrates the association between IDH mutation, immune exclusion, and disruptions in global DNA methylation. The melanoma-derived genomic data presented supports previously described resistance mechanisms of IDH mutation in other cancer types and is the first demonstration of the role of IDH GOF in the human melanoma tumor microenvironment.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-09DOI: 10.1172/jci.insight.199622
Claire Ross, Sanskruti Ravindra Gare, Nasser H Alatawi, Oveena Fonseka, Xinyi Chen, Jiayan Zhang, Yihua Han, Andrea Ruiz-Velasco, Riham Re Abouleisa, Yingjuan Liu, Xiangjun Zhao, Han Xiao, Bernard Keavney, Gareth J Howell, Tao Wang, Tamer Ma Mohamed, Elizabeth J Cartwright, Wei Liu
{"title":"Inhibition of calpain-mediated HMGB1 alleviates cardiac inflammation and dysfunction induced by ultra-processed foods.","authors":"Claire Ross, Sanskruti Ravindra Gare, Nasser H Alatawi, Oveena Fonseka, Xinyi Chen, Jiayan Zhang, Yihua Han, Andrea Ruiz-Velasco, Riham Re Abouleisa, Yingjuan Liu, Xiangjun Zhao, Han Xiao, Bernard Keavney, Gareth J Howell, Tao Wang, Tamer Ma Mohamed, Elizabeth J Cartwright, Wei Liu","doi":"10.1172/jci.insight.199622","DOIUrl":"https://doi.org/10.1172/jci.insight.199622","url":null,"abstract":"<p><p>Increased consumption of ultra-processed foods (UPFs) is a risk factor for metabolic disorders-associated heart failure (HF). Here, we demonstrate that UPF-induced calpain-1 aggravated oxidative stress, thereby increasing high mobility group box 1 (HMGB1)-mediated myocardial inflammation, which contributes to cardiac dysfunction. After illustrating the dysregulated inflammatory pathways in human and murine hearts upon metabolic stress, we revealed an increase in calpain-1 alongside profound oxidative stress and inflammation in the failing myocardium. Mechanistically, in neonatal rat cardiomyocytes (NRCMs) and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), HMGB1 was upregulated by calpain-1 and reactive oxygen species (ROS) upon stress of saturated and trans fatty acids (FA). Consequently, HMGB1 promoted a pro-inflammatory response in macrophages. On the contrary, inhibition of calpain or ROS efficiently repressed HMGB1 in cardiomyocytes. Therapeutically, either recombinant adeno-associated virus 9 (AAV9) delivered inhibitor of calpain-1 or its pharmacological inhibitor attenuated ROS and HMGB1-induced inflammation in the myocardium and mitigated HF in both male and female mice fed with an ultra-processed diet (UPD). Collectively, we have demonstrated the effects of suppressing calpain-1 and oxidative stress on alleviating myocardial inflammation via blockage of HMGB1 and cardiac dysfunction. The results provide a promising therapeutic strategy for preventing or treating HF in metabolic disorders.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147771531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-09DOI: 10.1172/jci.insight.194491
Stephan A Ramos, Preksha Bhagchandani, Diego M Burgos, Xueying Gu, Richard Rodriguez, Nadia Nourin, Martin Neukam, Shiva Pathak, Judith Shizuru, Seung K Kim
{"title":"Improved conditioning for hematopoietic chimerism induces islet tolerance to cure diabetes.","authors":"Stephan A Ramos, Preksha Bhagchandani, Diego M Burgos, Xueying Gu, Richard Rodriguez, Nadia Nourin, Martin Neukam, Shiva Pathak, Judith Shizuru, Seung K Kim","doi":"10.1172/jci.insight.194491","DOIUrl":"https://doi.org/10.1172/jci.insight.194491","url":null,"abstract":"<p><p>Mixed hematopoietic chimerism after hematopoietic cell transplantation (HCT) can modulate the immune system and induce tolerance to allogeneic tissues. However, bone marrow conditioning-related toxicities preclude wider adoption of HCT for transplant allotolerance. We sought agents that reduced conditioning intensity, while promoting durable mixed chimerism after HCT across complete major histocompatibility complex (MHC) mismatch in diabetic mice, permitting islet allotransplantation and diabetes reversal. We systematically tested baricitinib (JAK1/2 inhibitor), venetoclax (Bcl2 inhibitor), and αCD47 antibody, agents in current clinical use, and quantified hematopoietic chimerism after HCT. Combined with αCD117 antibody, transient T cell depletion, and just 10 centigray (cGy) total body irradiation (TBI), these agents enabled durable mixed chimerism and matching allo-islet tolerance, to cure diabetes without evidence of GVHD. Thus, we have developed a conditioning regimen to promote allogeneic mixed hematopoietic chimerism and transplanted islet allotolerance that minimizes conditioning radiation and cures diabetes, a significant achievement.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147771413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-09eCollection Date: 2026-05-08DOI: 10.1172/jci.insight.199827
Mona Chatrizeh, Jianmin Tian, Matthew Rogers, Firuz Feturi, Guojun Wu, Brian Firek, Roman Nikonov, Lauren Cass, Alexandra Sheppeck, Lavnish Ojha, Ali Carroll, Matthew Henkel, Justin Azar, Rajesh K Aneja, Brian Campfield, Dennis Simon, Michael J Morowitz
{"title":"Plant-based enteral nutrition outperforms ultra-processed formulas in mitigating consequences of antibiotic-induced dysbiosis.","authors":"Mona Chatrizeh, Jianmin Tian, Matthew Rogers, Firuz Feturi, Guojun Wu, Brian Firek, Roman Nikonov, Lauren Cass, Alexandra Sheppeck, Lavnish Ojha, Ali Carroll, Matthew Henkel, Justin Azar, Rajesh K Aneja, Brian Campfield, Dennis Simon, Michael J Morowitz","doi":"10.1172/jci.insight.199827","DOIUrl":"10.1172/jci.insight.199827","url":null,"abstract":"<p><p>Malnutrition, gut inflammation, and antibiotic-induced dysbiosis are well-recognized risk factors for poor clinical outcomes among critically ill patients. We previously showed that commercially available plant-based enteral nutrition (PBEN) preserves a commensal microbiome compared with commonly used artificial enteral nutrition (AEN). In this study, PBEN was superior to AEN in promoting recovery from antibiotic-induced dysbiosis in mice and humans. PBEN effectively mitigated anemia and leukopenia, restored naive lymphocyte populations, and reduced bone marrow myeloid expansion. Animals randomized to PBEN also exhibited improved responses to infectious gastrointestinal challenges following antibiotic exposure. A pilot clinical study validated these findings, demonstrating increased gut commensals, reduced pathogens, and improved leukocyte balance in critically ill children receiving PBEN compared with AEN. Together, these results suggest that PBEN offers a practical dietary approach to mitigate antibiotic-associated complications and potentially improve clinical outcomes among hospitalized patients requiring supplemental nutrition.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer.","authors":"Natsuki Nakagawa, Minemichi Toda, Akiko Kunita, Masafumi Horie, Masakatsu Tokunaga, Hiroaki Ikushima, Mirei Ka, Takahiro Iida, Manabu Shigeoka, Yukinobu Ito, Takahiro Ando, Kousuke Watanabe, Yasunori Ota, Xi Liu, Ethan Dmitrovsky, Hidenori Kage, Masanori Kawakami","doi":"10.1172/jci.insight.199352","DOIUrl":"10.1172/jci.insight.199352","url":null,"abstract":"<p><p>Supernumerary centrosomes are a hallmark of cancer. To maintain viability, cancer cells cluster these centrosomes during mitosis, enabling bipolar division similar to that of normal cells. Disruption of this centrosome clustering leads to multipolar anaphase and apoptosis (anaphase catastrophe), which selectively eliminates cancer cells harboring supernumerary centrosomes. In this context, because the motor protein KIFC1 contributes to centrosome clustering, we investigated whether targeting of this mechanism through KIFC1 inhibition could be exploited in small-cell lung cancer (SCLC), an aggressive malignancy with limited treatment options and poor prognosis. Through in silico and in vitro analyses, as well as IHC of clinical samples, we found that KIFC1 is overexpressed and that centrosome amplification occurs more frequently in SCLC compared with normal tissues and other cancer types. Pharmacological and genetic inhibition of KIFC1 disrupted the clustering of supernumerary centrosomes, triggered multipolar mitosis, and exerted antineoplastic effects in SCLC cells, with minimal effects on noncancerous cells. These findings were validated and extended in vivo using SCLC xenograft models. Finally, cotargeting KIFC1 and the centrosome duplication regulator PLK4 further enhanced growth suppression in SCLC cells. Together, these results suggest that disrupting centrosome clustering and triggering anaphase catastrophe via KIFC1 inhibition may represent a promising therapeutic strategy for SCLC.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 7","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Activation of SLIT2/ROBO1/LRP6 axis aggravates cartilage degradation via β-catenin signaling in TMJOA.","authors":"Guan Luo, Baoyi Chen, Wenjun Chen, Huiyi Lin, Weiqi Guo, Qingbin Zhang, Jiang Li, Lijing Wang, Janak Lal Pathak, Yuhui Yang, Weijun Zhang, Xiaoyu Zhang, Beining Zheng, Ziyi Wang, Shiting Wei, Jiaxin He, Wei-Jie Zhou, Chang Liu","doi":"10.1172/jci.insight.193632","DOIUrl":"10.1172/jci.insight.193632","url":null,"abstract":"<p><p>Temporomandibular joint osteoarthritis (TMJOA), a prevalent subtype of temporomandibular disorders, is characterized by progressive cartilage degradation and subchondral bone destruction. Despite advancements in understanding TMJOA pathogenesis, the molecular mechanisms underlying its progression remain unclear. In this study, elevated Slit guidance ligand 2 (SLIT2) expression was observed in TMJ tissues of unilateral anterior crossbite-induced TMJOA mice and synovial fluid from patients with TMJOA, correlating with disease severity. Furthermore, SLIT2 overexpression in transgenic mice intensified TMJOA progression, whereas heterozygous deletion of roundabout guidance receptor 1/2 (ROBO1/2) alleviated cartilage and bone damage. Mechanistically, SLIT2 promoted ROBO1-LRP6 complex formation, facilitating LRP6 phosphorylation and β-catenin nuclear translocation. This cascade upregulated matrix-degrading enzymes while downregulating cartilage structural proteins, exacerbating cartilage destruction and subchondral bone loss. These findings suggest that the SLIT2/ROBO1/LRP6 axis may represent a potential therapeutic target for TMJOA and provide mechanistic insights into disease progression.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 7","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-08DOI: 10.1172/jci.insight.201116
Andrew J Konecny, Fang Yun Lim, Eva Domenjo-Vila, Erika Lovas, Rachel L Blazevic, Louise E Kimball, Michael Boeckh, Alpana Waghmare, Martin Prlic
{"title":"An at-home blood collection device for remote immune monitoring by high-parameter flow cytometry.","authors":"Andrew J Konecny, Fang Yun Lim, Eva Domenjo-Vila, Erika Lovas, Rachel L Blazevic, Louise E Kimball, Michael Boeckh, Alpana Waghmare, Martin Prlic","doi":"10.1172/jci.insight.201116","DOIUrl":"10.1172/jci.insight.201116","url":null,"abstract":"<p><p>At-home blood collection devices (ABCDs) can facilitate study participation for remote and rural cohorts. Previous studies used ABCDs to interrogate samples by proteomics and sequencing approaches. We wanted to address the question of whether this approach could be used to assess live immune cells with high-parameter flow cytometry to enable remote immune monitoring. We first compared blood from standard venipuncture with ABCD blood draws, followed by assessment of the impact of sample shipping on immune cell viability and phenotyping. We found that capillary blood collected with a Tasso+ device and concurrently drawn venipuncture blood samples had highly congruent immune cell composition and phenotype. Shipment of Tasso+ samples via the United States Postal Service altered the myeloid compartment, but T cell numbers, subsets, and phenotypes remained remarkably stable compared with non-shipped samples. Finally, we describe a flow cytometry analysis framework that allowed for direct sample comparison even when samples were stained and analyzed over a time period of 1.5 years. Overall, our data highlight the feasibility of using ABCDs combined with subsequent flow cytometry analysis for remote immune monitoring. Additionally, our study also identifies areas that could be improved to further promote the use of ABCDs for immune monitoring.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 7","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-08DOI: 10.1172/jci.insight.197470
Qiuheng Tian, Han Liu, Xiang Gu, Jing Shen, Xi Yuan, Mengqi Zheng, Yunjiao Zhai, Yatai Chen, Penghu Han, Yangchun Ma, Wei Xin, Hongyue Ma, Yu Li, Sihan Wang, Lei Guo, Detian Yuan, Yanbo Yu, Shiyang Li
{"title":"Vancomycin eliminates gut deoxycholic acid, restoring ER proteostasis in ILC2s and relieving colitis.","authors":"Qiuheng Tian, Han Liu, Xiang Gu, Jing Shen, Xi Yuan, Mengqi Zheng, Yunjiao Zhai, Yatai Chen, Penghu Han, Yangchun Ma, Wei Xin, Hongyue Ma, Yu Li, Sihan Wang, Lei Guo, Detian Yuan, Yanbo Yu, Shiyang Li","doi":"10.1172/jci.insight.197470","DOIUrl":"10.1172/jci.insight.197470","url":null,"abstract":"<p><p>Ulcerative colitis (UC) remission is marked by gut microbiota restructuring, but how microbial metabolites influence immune-mediated tissue repair is unclear. Here, we demonstrate that oral vancomycin alleviates colitis symptoms in murine models, mirroring its clinical efficacy in inducing remission in patients with UC. Mechanistically, vancomycin's therapeutic effect is achieved by reducing deoxycholic acid (DCA). We reveal that DCA impairs mucosal repair driven by group 2 innate lymphoid cells (ILC2s) by inducing ER stress through direct binding to thioredoxin-related transmembrane protein 2 (TMX2). This interaction disrupts TMX2's role in protein folding, triggering unresolved unfolded protein response via hyperactivation of PERK/eIF2α signaling, which suppresses the production of pro-healing molecules by ILC2s. Pharmacological inhibition of PERK phosphorylation restores ILC2 function and accelerates colitis resolution. Our work uncovers a pathogenic microbiota/DCA/ILC2 axis that obstructs mucosal healing and positions vancomycin as a targeted strategy to eliminate DCA, thereby promoting UC remission.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 7","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-08DOI: 10.1172/jci.insight.202639
Lori A Birder, Amanda Wolf-Johnston, Jonathan Franks, Mara Lg Sullivan, Simon C Watkins, Anthony J Kanai, Vladimir B Ritov, Edwin K Jackson
{"title":"8-Aminoguanine protects against paclitaxel-induced neural degeneration and mechanical allodynia.","authors":"Lori A Birder, Amanda Wolf-Johnston, Jonathan Franks, Mara Lg Sullivan, Simon C Watkins, Anthony J Kanai, Vladimir B Ritov, Edwin K Jackson","doi":"10.1172/jci.insight.202639","DOIUrl":"10.1172/jci.insight.202639","url":null,"abstract":"<p><p>Current treatment protocols for most types of cancers require chemotherapeutic agents that are associated with significant side effects, including chemotherapy-induced peripheral neuropathy (CIPN). Currently, there are no effective CIPN prevention strategies, and current treatment approaches remain limited. The enzyme purine nucleoside phosphorylase (PNPase) actively modulates both oxidative injury and cellular damage. Here, we tested the hypothesis that the signs and symptoms of CIPN are due to a chemotherapy-induced dysregulation of the purine metabolome. We assessed the effect of PNPase inhibition on paclitaxel-induced (PAC-induced) CIPN. Female adult Sprague-Dawley rats were treated with PAC and randomized to oral treatment with either the PNPase inhibitor 8-aminoguanine (8-AG) or its vehicle. Some rats were injected with shRNA against PNPase prior to PAC injections. PAC-treated rats exhibited multiple abnormalities: mechanical allodynia and changes in damaging purines, intraepidermal nerve fiber (IENF) density, and signaling cascades involved in mitochondrial disruption and axonal damage. Inhibition of PNPase improved behavioral function (mechanical allodynia), rescued the loss/damage of IENF, and normalized markers for mitochondrial dysfunction and nerve damage. These findings support the hypothesis that inhibition of PNPase prevented (and potentially reversed) CIPN through several mechanisms that included a reduction in neuronal damage and development of mechanical allodynia.</p>","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 7","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JCI insightPub Date : 2026-04-08DOI: 10.1172/jci.insight.206548
Eduardo Vieira Neto, Meicheng Wang, Austin J Szuminsky, Lethicia Ferraro, Erik Koppes, Yudong Wang, Clinton Van't Land, Al-Walid Mohsen, Geancarlo Zanatta, Areeg H El-Gharbawy, Tamil S Anthonymuthu, Yulia Y Tyurina, Vladimir A Tyurin, Valerian Kagan, Hülya Bayır, Jerry Vockley
{"title":"Corrigendum to: Mitochondrial bioenergetics and cardiolipin remodeling abnormalities in mitochondrial trifunctional protein deficiency.","authors":"Eduardo Vieira Neto, Meicheng Wang, Austin J Szuminsky, Lethicia Ferraro, Erik Koppes, Yudong Wang, Clinton Van't Land, Al-Walid Mohsen, Geancarlo Zanatta, Areeg H El-Gharbawy, Tamil S Anthonymuthu, Yulia Y Tyurina, Vladimir A Tyurin, Valerian Kagan, Hülya Bayır, Jerry Vockley","doi":"10.1172/jci.insight.206548","DOIUrl":"10.1172/jci.insight.206548","url":null,"abstract":"","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 7","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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