tbuckley/cabot-search huggingface dataset:
Abstract P3-14-10: Intralesional steroid injection: A novel method to treat the symptoms of idiopathic granulomatous mastitis
Authors: DJ Manst, PS Ganschow, EA Marcus, C Holden, S Datta
Journal: Cancer Research (2019)

Abstract Background: Idiopathic granulomatous mastitis (IGM) is a chronic, inflammatory breast condition of benign nature that can clinically mimic breast cancer. Patients frequently present with a large, painful breast mass with associated inflammatory changes of the skin, and possible ulceration or fistula of the breast. Attempted methods for symptomatic relief include surgical excision and medical therapies including oral corticosteroids. Due to the success of treating dermatologic conditions with intralesional steroid injections, it was hypothesized that injecting the subdermal lesions of IGM may benefit patients with this disease. The use of intralesional steroid injections for the treatment of IGM has not been previously described in the literature. Methods: Retrospective chart review was performed on a series of four patients with IGM who received intralesional steroid injections between August 2017 and April 2018. Patients were selected for treatment with injections based on their subjective report of painful breast lesions, lesion characteristics including size and depth, and the patient's desire to stop oral steroid therapy due to side effects despite active or residual disease. Data were collected on demographics, initial physical examination findings, prior and current treatments, characteristics of disease, details of injections performed, objective and subjective response to treatment, and recurrence. Results: All patients presented with breast pain and either a mass, swelling, or hardness of the breast. Each patient received between one and three injection treatments, with one to four lesions treated in each session. Patients demonstrated improvement in subjective and objective symptoms after 87.5% of injection sessions (7 out of 8) by the subsequent follow-up visit (21-34 days). During the study period, three patients experienced resolution of at least one breast lesion within about 2 months (31-139 days, mean 68 days) without recurrence. One patient had four breast lesions that completely resolved (35-217 days, mean 88 days), but three of them recurred (63-217 days, mean 149 days). Conclusion: In a small group of patients with idiopathic granulomatous mastitis, intralesional steroid injections were associated with an improvement in both subjective symptomatic relief and objective breast lesion characteristics in most cases. This treatment was associated with a good rate of lesion resolution and a low short-term recurrence rate. Citation Format: Manst DJ, Ganschow PS, Marcus EA, Holden C, Datta S. Intralesional steroid injection: A novel method to treat the symptoms of idiopathic granulomatous mastitis [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P3-14-10.
CONCURRENT SURGICAL LEFT ATRIAL APPENDAGE OCCLUSION AND CORONARY ARTERY BYPASS GRAFT PROCEDURE IN PATIENTS WITH ATRIAL FIBRILLATION YIELDS NO ADDITIONAL RISK FOR ALL-CAUSE IN-HOSPITAL ADVERSE EVENTS: A NATIONWIDE STUDY
Authors: Ashraf Abugroun, Hakeem Ayinde, Raghav Chandra, Mikhael El Chami, Lloyd W. Klein
Journal: Journal of the American College of Cardiology (2019)
CARDIAC DEVICE DATA ANALYTICS AIDS IN IDENTIFICATION OF PATIENTS AT HIGH RISK FOR DECOMPENSATED SYSTOLIC HEART FAILURE
Authors: Rohit Mehta, Terri Cooper, Elizabeth Davenport, Seema Gupta, J. Jason Sims, Kathleen McCauley, Robin Leahy, Sanjeev Gulati
Journal: Journal of the American College of Cardiology (2019)
LEISURE TIME PHYSICAL ACTIVITY AFTER INVASIVE TREATMENT FOR SYMPTOMATIC PERIPHERAL ARTERY DISEASE: INSIGHTS FROM THE PORTRAIT REGISTRY
Authors: Poghni Peri-Okonny, Ali Malik, Jeremy Provance, Vittal Hijjaji, Kensey Gosch, John A. Spertus, Kim Smolderen
Journal: Journal of the American College of Cardiology (2019)
CLINICAL CHARACTERISTICS OF PERIPARTUM CARDIOMYOPATHY COMPARED TO PREECLAMPSIA
Authors: Ali Alkhayru, Bassman Tappuni, Belal Kaseer, Freidoon Ghazi, John Wilson, Kathleen Smith, William Schnettler, Jenni Steinbrunner, Kamal Shemisa
Journal: Journal of the American College of Cardiology (2019)
Metabolism Drives Carcinogenesis and Maintenance of Pancreatic Tumors
Authors: Christopher J. Halbrook, Barbara S. Nelson, Costas A. Lyssiotis
Journal: Cancer Discovery (2019)

Abstract Summary: In this issue of Cancer Discovery, Carrer and colleagues find that early events in pancreatic tumorigenesis are driven by altered acetyl-CoA metabolism, where targeting this axis in established cancer models impairs tumor growth. This work provides new insights into the roles of acetyl-CoA in pancreatic cancer and underscores the value of studying early events in carcinogenesis to yield new treatment strategies. See related article by Carrer et al., p. 416.
Just a cutaneous (keratotic) horn?
Authors: Jane Wilcock, Yvonne Savage
Journal: BMJ (2019)

A 70 year old woman attended a dermatologist with a lesion on the dorsum of her right hand (fig 1). It had appeared over eight weeks and was painless but unsightly. She reported good health and no history of warts. Fifteen years ago, she had lymphoma treated by chemotherapy; her last treatment (biological therapy) had finished seven years ago and she had been well since. She had holidayed in Australia for three months at a time over the last three years and more recently had driven frequently from northern England to the south coast while a close relative was ill. She said she was careful to use sunscreen.



Fig 1 
Keratotic horn lesion on dorsum of the right hand



The lesion had a red, firm base 2 × 1 cm and 3 mm with a cutaneous horn protruding another 5 mm.

She had cryocautery twice by her general practitioner which did not alter the lesion and so chose to attend a private dermatologist. The lesion was excised.

What is the most likely diagnosis?

Invasive squamous cell cancer masquerading as keratotic horn.

A keratotic horn is derived from the superficial keratinocyte layer of the skin.

Differential diagnoses include seborrheic keratosis (seborrheic wart); human papilloma virus (HPV) wart and keratoacanthoma (benign); actinic keratosis, which is pre-malignant; Bowen’s disease, which is a non-invasive squamous cell …
Abstract 413: NAD <sup>+</sup> -dependent Pathogenic Mechanisms and Metabolic Interventions for Mitochondrial Disease and its Associated Cardiomyopathy
Authors: Chi Fung Lee, Arianne Caudal, Lauren Abell, G. A. Nagana Gowda, Rong Tian
Journal: Circulation Research (2018)

Leigh syndrome (LS) is a congenital mitochondrial disease. Patients with LS develop metabolic abnormality and progressive dysfunctions in brain, skeletal and cardiac muscles, eventually leading to early death. A mouse model of LS with deficiency of a Complex I subunit, Ndufs4-null mice (KO), was used in this study. Depleted NAD + level and NAD + redox imbalance were observed in KO brain and lead to inhibitions of poly (ADP-ribose) polymerase (PARP)-dependent DNA repair and SOD2 activity via protein hyperacetylation. These inhibitions promoted oxidative stress and increased H2Ax phosphorylation, a DNA damage marker, leading to neurological impairments in KO. To counteract the NAD + depletion associated with the pathogenesis of KO, we targeted NAD + salvage pathway to increase NAD + pool size. Supplementation of nicotinamide mononucleotide (NMN), a NAD + precursor, doubled lifespan of KO mice from 55 to 110 days, but did not attenuate neurological impairments, owing to the failure to elevate NAD + levels in brain. We next determined the underlying mechanisms by which NMN extended lifespan of KO without impacting brain NAD + pool. NMN elevated NAD + levels in skeletal and cardiac muscles of KO, resulting in blunted hyperacetylation and attenuated systolic dysfunction. NMN lowered lactate levels in serum and muscles of KO, associated with suppression of hypoxic signaling (lowered HIF1α, LDHA levels). The data suggest a NAD + -sensitive mechanism that suppresses glycolysis in KO treated by NMN via hypoxic signaling. While acetylation levels of HIF1α protein were unchanged in KO, acetylation of glutamate dehydrogenase (GDH) was upregulated in KO and suppressed by NMN. Deacetylation of GDH after NMN treatment promoted upregulation of α-ketoglutarate (KG) level in KO, a co-substrate needed for HIF1α degradation. The results suggested that KG may be beneficial to KO. To determine the therapeutic potential of KG, dimethyl-ketoglutarate (DMKG), a cell permeable form of KG, was administered to KO. DMKG extended lifespan and improved systolic function in KO, associated with suppressed hypoxic signaling. Collectively, this study identified NAD + -dependent pathogenic mechanisms that may lead to translatable interventions for LS and mitochondrial cardiomyopathy.
UPPER GASTROINTESTINAL BLEEDING IS ASSOCIATED WITH SIGNIFICANT MORTALITY IN PATIENTS UNDERGOING PERCUTANEOUS CORONARY INTERVENTION FOR STABLE ISCHEMIC HEART DISEASE
Authors: Fawad Virk, Muhammad Choudhry, Hussain Ibrahim, Wissam Khalife, Umamahesh Rangasetty, Syed Gilani
Journal: Journal of the American College of Cardiology (2019)
Management of Post-transplant Hyperparathyroidism and Bone Disease
Authors: Rowena Delos Santos, Ana Rossi, Daniel Coyne, Thin Thin Maw
Journal: Drugs (2019)

Significant advances in immunosuppressive therapies have been made in renal transplantation, leading to increased allograft and patient survival. Despite improvement in overall patient survival, patients continue to require management of persistent post-transplant hyperparathyroidism. Medications that treat persistent hyperparathyroidism include vitamin D, vitamin D analogues, and calcimimetics. Medication side effects such as hypocalcemia or hypercalcemia, and adynamic bone disease, may lead to a decrease in the drugs. When medical management fails to control persistent post-transplant hyperparathyroidism, treatment is a parathyroidectomy. Surgical techniques are not uniform between centers and surgeons. Undergoing the surgery may include a subtotal technique or a technique including total parathyroid gland resection with partial heterotopic gland reimplantation. In addition, there are possible post-surgical complications. The ideal treatment for persistent post-transplant hyperparathyroidism is the treatment and prevention of the condition while patients are being managed for their late-stage chronic kidney disease and end-stage renal disease.
THE IMPACT OF BLEEDING AVOIDANCE STRATEGIES IN MEN AND WOMEN UNDERGOING PERCUTANEOUS CORONARY INTERVENTION
Authors: Navjot Kaur Sobti, David Malenka, Peter N. Ver Lee, Rony Lahoud, Yi-Ling Huang, Thomas J. Ryan, James M. Flynn, Patrick Magnus, Bina Ahmed
Journal: Journal of the American College of Cardiology (2019)
Impact of Newer Agents on Progression Free Survival of Multiple Myeloma in the 2nd 3rd and 4th Line Setting- a Systematic Review
Authors: Muhammad Sardar, Jemin Aby Jose, Zunairah Shah, Chaudhry Saad Sohail, Insija Ilyas Selene, Madeeha Shafqat, Anum Qureshi, Raza Naseer, Ali Younas Khan, Saad Ullah Malik, Faiz Anwer
Journal: Blood (2018)
TIME-INTEGRATED AORTIC REGURGITATION INDEX HELPS IN THE REAL-TIME ASSESSMENT OF PARAVALVULAR REGURGITATION DURING TAVR
Authors: Arnav Kumar, Kimi Sato, Yash Jobanputra, Jorge Betancor, Mohamed Halane, Robin George, Kinjal Banerjee, Divyanshu Mohananey, Vivek Menon, Yasser Sammour, Amar Krishnaswamy, Wael Jaber, Stephanie Mick, Lars Svensson, Samir Kapadia
Journal: Journal of the American College of Cardiology (2019)
Abstract 209: Downregulation of KLF2 in the Endothelium Contributes to the Pathogenesis in LMNA-related Dilated Cardiomyopathy
Authors: Nazish Sayed, Chun Liu, Farhan Himmati, Joe Zhang, Saereh Khanamiri, Haodong Chen, Jan-Ranier Moonen, Alexa Wnorowski, Elena Matsa, Linling Cheng, Karim Sallam, Marlene Rabinovitch, Joseph C Wu
Journal: Circulation Research (2018)

Background: Mutations in the gene that encodes the nuclear envelope proteins lamin A and C (LMNA) accounts for 6% of all cases of Dilated Cardiomyopathy (DCM). However, the molecular mechanisms that underlie “cardiolaminopathy” remain elusive, and it is unknown why mutations in this ubiquitously expressed gene have such a disproportionate effect on the heart. Hypothesis: Despite the fact that LMNA is abundantly expressed in endothelial cells (ECs) and mutations in LMNA are known to induce EC dysfunction, little is known about the EC-specific phenotype of LMNA-related DCM. As EC dysfunction has been known to contribute to DCM, we hypothesize that EC dysfunction due to LMNA mutation has a significant impact on the pathogenesis and disease progression of DCM. Results: Intriguingly, our preliminary data showed that iPSC-ECs derived from patients (n=5) harboring the LMNA-mutation exhibit decrease functionality as seen by impaired angiogenesis and decreased NO production (control iPSC-ECs vs LMNA iPSC-ECs; p&lt;0.05). Similarly, genome editing of isogenic iPSC lines enabled us to recapitulate the EC disease phenotype further allowing us to dissect the effects of LMNA mutations on EC function. LMNA corrected iPSC-ECs (via use of CRISPR/Cas9 genome editing tool to correct the single mutated copy in heterozygous patient’s iPSCs) showed restoration of EC function. Whole genome RNA-sequencing identified Krüppel-like Factor 2 (KLF2) as a potential transcript responsible for EC dysfunction in LMNA-mutated patients. Importantly, treatment of LMNA-mutated ECs with KLF2 agonists showed rescue of EC dysfunction. Furthermore, iPSC-derived cardiomyocytes (iPSC-CMs) from LMNA-mutated patients that exhibited DCM phenotype, showed improvement in CM physiology when co-cultured with iPSC-ECs treated with KLF2 agonists. Conclusion: This study is a first step towards understanding the molecular mechanisms of cardiolaminopathy by modeling endothelial dysfunction using patient-specific iPSCs. Moreover, our results suggest that improving EC function in cardiolaminopathy patients could have a significant impact on the pathogenesis of DCM. Results from this work could potentially lead to new strategies that could improve the management of DCM patients.
EOSINOPHILIC MYOCARDITIS: A CASE REPORT OF MYOCARDITIS AS THE INITIAL PRESENTATION OF EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS
Authors: Pratik Mondal, Kartik Dhaduk, Srikanth Yandrapalli, Avi Levine, Wilbert Aronow
Journal: Journal of the American College of Cardiology (2019)
Atrophic acne scar: a process from altered metabolism of elastic fibres and collagen fibres based on transforming growth factor‐β1 signalling
Authors: J. Moon, J.Y. Yoon, J.H. Yang, H.H. Kwon, S. Min, D.H. Suh
Journal: British Journal of Dermatology (2019)

Atrophic acne scar, a persistent sequela from acne, is undesirably troubling to many patients due to its cosmetic and psychosocial aspects. Although there have been some reports emphasizing the role of early inflammatory responses in atrophic acne scarring, evolving perspectives on the detailed pathogenic processes are promptly needed. Examining the histological, immunological and molecular changes in early acne lesions susceptible to atrophic scarring can provide new insights to understand the pathophysiology of atrophic acne scar. We experimentally validated several early fundamental hallmarks accounting for the transition of early acne lesions to atrophic scars by comparing molecular profiles of skin and acne lesions between patients who were prone to scar (APS) or not (ANS). In APS, compared with ANS, devastating degradation of elastic fibres and collagen fibres occurred in the dermis, followed by their incomplete recovery. Abnormally excessive inflammation mediated by innate immunity with T helper 17 and T helper 1 cells was observed. Epidermal proliferation was significantly diminished. Transforming growth factor (TGF)‐β1 was drastically elevated in APS, suggesting that aberrant TGF‐β1 signalling is an underlying modulator of all of these pathological processes. These results may provide a basis for understanding the pathogenesis of atrophic acne scarring. Reduction of excessive inflammation and TGF‐β1 signalling in early acne lesions is expected to facilitate the protection of normal extracellular matrix metabolism and ultimately the prevention of atrophic scar formation. What's already known about this topic? The dermis of atrophic acne scars shows alteration of extracellular matrix components such as collagen fibres. Inflammation in acne lesions is associated with the development of acne scars. What does this study add? Abnormalities in the metabolism of collagen fibres and elastic fibres were observed in the early developmental stages of acne lesions that were progressing into atrophic scars. Exacerbated inflammation and aberrant epidermal proliferation by increased transforming growth factor (TGF)‐β1 signalling may affect the abnormal extracellular matrix metabolism. What is the translational message? Abnormal changes in elastic fibres and collagen fibres are found in the early developmental process of acne in patients who are prone to atrophic scarring. An early treatment regimen strongly inhibiting inflammation and TGF‐β1 signalling to help the normal recovery of the extracellular matrix components is required to prevent atrophic scarring.
RESTRICTIVE CARDIOMYOPATHY TYPE C AND LEFT VENTRICULAR NON-COMPACTION: A RARE ASSOCIATION
Authors: Nilda Espinola-Zavaleta, Diego Oregel Oregel-Camacho, Erick Alexanderson-Rosas, Alondra Flores-Garcia, Gyselle Camacho-Camacho
Journal: Journal of the American College of Cardiology (2019)
CHOLESTEROL CRYSTAL PENETRATING FIBROUS CAP AS A NEW INDEPENDENT PREDICTOR FOR PLAQUE RUPTURE
Authors: Yosuke Katayama, Atsushi Tanaka, Manabu Kashiwagi, Kunihiro Shimamura, Yasutsugu Shiono, Yoshiki Matsuo, Yasushi Ino, Hironori Kitabata, Takashi Kubo, Takeshi Hozumi, Takashi Akasaka
Journal: Journal of the American College of Cardiology (2019)
PROGNOSTIC IMPACT OF RIGHT VENTRICULAR DYSFUNCTION IN PATIENTS WITH ADVANCED ISCHEMIC CARDIOMYOPATHY: SEX-RELATED DIFFERENCES
Authors: Ramya Vajapey, Natalie Ho, Julijana Conic, Nancy Obuchowski, Nathanial Lee, Sophia Downey, Leslie Cho, Brian Griffin, Scott Flamm, Wilson Tang, Deborah Kwon
Journal: Journal of the American College of Cardiology (2019)
TRENDS OF PULMONARY ARTERY CATHETER USE IN HEART FAILURE HOSPITALIZATIONS: A NATIONAL ESTIMATE
Authors: Mandira Patel, Srishti Nayak, Prashant Patel, Amish Patel, Kishore Mukherjee, Steven Deutsch, Sami Nazzal, Issa Alesh
Journal: Journal of the American College of Cardiology (2019)
DOES AN IMPLANTABLE DEFIBRILLATOR ALTER OUTCOMES IN PATIENTS WITH CARDIAC AMYLOIDOSIS?
Authors: Eun Jeong Kim, Benjamin Holmes, Shi Huang, Ricardo Lugo, Asad Al Aboud, Travis Richardson, Stacey Goodman, Rebecca R. Hung, David Slosky, William Stevenson, Gregory Michaud, Roy John
Journal: Journal of the American College of Cardiology (2019)
Preliminary Results of a Phase I Study of Obinutuzumab, Venetoclax, and Lenalidomide in Relapsed and Refractory B-Cell Non-Hodgkin Lymphoma
Authors: Kami J. Maddocks, Farrukh T. Awan, Ying Huang, Sabarish Ayyappan, Robert A Baiocchi, Narendranath Epperla, Samantha Jaglowski, Basem M. William, Kristie A. Blum, Beth A. Christian
Journal: Blood (2018)
IMPACT OF MODERATE/SEVERE MITRAL REGURGITATION ON 2-YEAR OUTCOMES AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT IN THE REPRISE III RANDOMIZED CONTROLLED TRIAL
Authors: Stephen Little, Mani Vannan, Siddharth Singh, Bijoy Khandheria, Dominic Allocco, Ted Feldman, Neil Weissman, Federico Asch
Journal: Journal of the American College of Cardiology (2019)
IDENTIFYING PREDICTORS OF HOSPITALIZATION DUE TO HEART FAILURE IN THE TOPCAT TRIAL USING MACHINE LEARNING TECHNIQUES
Authors: Gauri Dandi, Amit Dey, Yuan Gu, Ruba Shalhoub, Runqiu Wang, Colin Wu, Xin Tian, Eileen Navarro Almario, Tejas Patel, Jerome Fleg, Anna Kettermann, Gyorgy Csako, George Sopko, Helena Sviglin, Nashwan Farooque, Zyannah Mallick, Victoria Xin, Laboni Hoque, Iffat Chowdhury, Keith Burkhart, Lawton Cooper, Nehal Mehta, Frank Pucino, Yves Rosenberg, Ahmed Hasan
Journal: Journal of the American College of Cardiology (2019)
A protein-interaction network of interferon-stimulated genes extends the innate immune system landscape
Authors: Philipp Hubel, Christian Urban, Valter Bergant, William M. Schneider, Barbara Knauer, Alexey Stukalov, Pietro Scaturro, Angelika Mann, Linda Brunotte, Heinrich H. Hoffmann, John W. Schoggins, Martin Schwemmle, Matthias Mann, Charles M. Rice, Andreas Pichlmair
Journal: Nature Immunology (2019)
LONG TERM OUTCOMES OF TRANSCATHETER AORTIC VALVE REPLACEMENT VERSUS SURGICAL AORTIC VALVE REPLACEMENT FOR INTERMEDIATE SURGICAL RISK PATIENTS: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Garly Rushler Saint Croix, Soluny Jean, Michel Ibrahim, Beteal Ashinne, Alexander Toirac, Jennifer Maning, Eduardo de Marchena
Journal: Journal of the American College of Cardiology (2019)
APPLICATION OF TICAGRELOR OR CLOPIDOGREL BASED DUAL ANTIPLATELET THERAPY FOLLOWING A PHARMACOINVASIVE STRATEGY IN ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION: INSIGHTS FROM THE VITAL HEART RESPONSE REGISTRY
Authors: Robert C. Welsh, Jay Shavadia, Yinggan Zheng, Benjamin Tyrrell, Raymond Leung, Neil Brass, Kevin Bainey
Journal: Journal of the American College of Cardiology (2019)
EFFECT OF SACUBITRIL/VALSARTAN ON BIOMARKERS OF MYOCARDIAL STRESS IN PATIENTS HOSPITALIZED WITH ACUTE HEART FAILURE IN PIONEER-HF
Authors: David A. Morrow, Eric Velazquez, Adam DeVore, Carol I. Duffy, Margaret Prescott, Kevin McCague, Ricardo Rocha, Eugene Braunwald
Journal: Journal of the American College of Cardiology (2019)
Abstract 317: Nlrc5 Positively Regulates Intimal Formation via Interaction With PPARã in Vascular Smooth Muscle Cells
Authors: Jianhui Zhuang, Peipei Luan, Yawei Xu, Wenhui Peng
Journal: Circulation Research (2018)

Background: Innate immunity and vascular smooth muscle cells play crucial role in the development of vascular remodeling and intimal hyperplasia. NLR family CARD domain containing 5 (Nlrc5), known as a pattern recognition receptor, has been noted for its implication in immune disease in recent studies. However, whether Nlrc5 regulates intimal hyperplasia is still unclear. Aim: We aimed to determine the role of Nlrc5 in intimal hyperplasia and its underlying molecular mechanism. Methods and Results: We showed that an elevated expression of Nlrc5 in neointima induced by carotid ligation compared normal carotid artery. In human aortic smooth muscle cells (HASMCs), PDGF induced Nlrc5 expression and nuclear translocation. By utilizing Nlrc5 knockout mice, we found Nlrc5 deficiency prominently aggravated neointimal formation compared to wild type (WT) mice. On the contrary, gain of function of Nlrc5 based on local adenovirus injection attenuated intimal hyperplasia. The neointimal area was comparable in WT mice receiving either WT or Nlrc5-/- bone marrow transplantation, demonstrating that hematopoietic cell-derived Nlrc5 did not affect vascular hyperplasia. In vitro experiments unveiled that knockdown of Nlrc5 resulted in excessive proliferation, migration and dedifferentiation of HASMCs. Nevertheless, depletion of Nlrc5 in HASMCs did not influence proinflammatory cytokine excretion and immune activation reflected by major histocompatibility complex-I expression. Mechanistic study revealed that Nlrc5 bound to nuclear transcription factor PPARγ and positively regulated PPARγ luciferase activity, ensuing contributing to KLF4 ubiquitination and degradation. Furthermore, we generated five deletion constructs of Nlrc5 and identified that the functional domain containing DD and NACHT constructs was responsible for the interaction with PPARγ. Conclusions: Our study reveals that Nlrc5 alleviates intimal formation through interaction with PPARγ and inhibition of smooth muscle cell dedifferentiation, suggesting that Nlrc5 constitutes a novel molecular target for vascular remodeling.