Omentin-1 protein has protective effects against coronary artery disease (CAD). The Val109Asp polymorphism (rs2274907) in the Omentin-1 gene has been associated with CAD risk, but this relationship has not been investigated in patients with type 2 diabetes mellitus (T2DM). To investigate the association between the Omentin-1 Val109Asp polymorphism and CAD risk in Han Chinese patients with T2DM. This case-control study enrolled 465 Han Chinese patients with T2DM from July 2008 to September 2015. Participants were classified as CAD-positive (coronary stenosis > 50% in at least 1 major vessel, n = 249) or CAD-negative (n = 216). The Val109Asp polymorphism was genotyped using PCR-RFLP. Logistic regression analysis was performed to assess the association between genotypes and CAD risk, with adjustment for potential confounders including age, sex, smoking status, hypertension, dyslipidemia, diabetes duration, body mass index, and fasting glucose. The A allele frequency was higher in CAD patients than in controls (34.5% vs 27.5%; OR = 1.386; P = .026). Under the dominant model, TA/AA carriers had increased CAD risk compared with TT homozygotes (adjusted OR = 1.509, 95% CI: 1.025-2.222; P = .037). Stratified analyses showed that smokers carrying the A allele exhibited further elevated CAD risk (adjusted OR = 1.82, 95% CI: 1.02-3.27). The Omentin-1 Val109Asp polymorphism is associated with increased CAD risk in Han Chinese patients with T2DM under the dominant genetic model. Stratified findings suggest that smoking may further heighten CAD susceptibility among A-allele carriers. Integrating genetic and lifestyle factors may improve cardiovascular risk assessment in this population.

BACKGROUND:Left ventricular hypertrophy (LVH) is a critical complication of hypertension that correlates with increased morbimortality. Its pathophysiology is complex and multifaceted likely involving various players that are still to be determined, particularly those with proinflammatory and profibrotic effects. Complement C1q/tumour necrosis factor-related protein 1 (CTRP1) is an antihypotensive adipokine that has recently been linked to adverse cardiometabolic changes and may contribute to the development of LVH. OBJECTIVE:To explore the relationship between CTRP1 and LVH in patients with essential hypertension. METHODS:A total of 360 patients with mild-to-moderate essential hypertension were enrolled from Ruijin Hospital between December 2015 and November 2017. Participants were divided into two groups: those with hypertension alone (n = 183) and those with hypertension complicated by LVH (n = 177). Plasma levels of CTRP1, adiponectin, and interleukin-6 (IL-6) were measured using enzyme-linked immunosorbent assay (ELISA). The left ventricular mass index (LVMI) was calculated from echocardiographic measurements. Patients were further stratified by sex and by CTRP1 tertiles for subgroup analysis. RESULTS:Patients with hypertension and LVH showed significantly higher levels of CTRP1, IL-6, and LVMI compared to those with hypertension alone. In contrast, adiponectin levels were significantly lower in the LVH group. CTRP1 levels were positively correlated with LVMI in both males and females. Furthermore, patients in the highest CTRP1 tertile exhibited progressively elevated SBP, DBP, CRP, IL-6, and LVMI. Multivariate logistic regression analysis identified CTRP1, IL-6, and adiponectin as independent factors associated with LVH. CONCLUSION:CTRP1 is independently associated with left ventricular hypertrophy in patients with essential hypertension, demonstrating a dose-response relationship with cardiac hypertrophy and inflammatory markers.

Background Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with profound metabolic rewiring and resistance to therapy. Sodium-glucose co-transporter 2 (SGLT2) regulates glucose uptake, but its role in PDAC remains unclear. Methods SGLT2 expression was analyzed in clinical samples and public datasets. PDAC cell lines were subjected to genetic knockdown or canagliflozin (CANA) treatment to assess proliferation, migration, apoptosis, and glucose metabolism. Mechanistic studies investigated AMPK-ULK1 signaling, autophagy dynamics, oxidative stress, and EGFR signaling. Xenograft models were used to assess in vivo efficacy. Results SGLT2 was upregulated in PDAC and associated with poor prognosis. SGLT2 inhibition suppressed proliferation and migration while promoting apoptosis. Mechanistically, CANA induced ATP deficiency and initiated autophagy, but concurrently impaired autophagosome-lysosome fusion. This dual effect led to autophagic flux blockade, resulting in excessive ROS accumulation, mitochondrial dysfunction, and apoptosis. Inhibition of AMPK reduced ROS levels, while ROS scavenging partially rescued mitochondrial damage and cell death. Notably, SGLT2 inhibition enhanced sensitivity to EGFR-targeted therapy, producing synergistic anti-tumor effects in vitro and in vivo. Conclusions SGLT2 maintains metabolic and autophagic homeostasis in PDAC. Its inhibition induces metabolic stress, autophagic flux blockade, and ROS-driven mitochondrial apoptosis. In addition, targeting SGLT2 sensitizes tumors to EGFR-targeted therapy, offering a novel combinatorial strategy.

Background Several studies have suggested that N6‐methyladenosine (m6A) plays an essential role in cardiovascular disease, but the causality of m6A on ischemic heart disease (IHD) remains unknown. Therefore, this study investigated the potential relationship between m6A and IHD using a 2‐sample Mendelian randomization method. Methods The publicly available genome‐wide association study data for m6A‐related proteins were obtained from the INTERVAL study, a large population‐based cohort of healthy blood donors in the United Kingdom, whereas the genome‐wide association study database (including 30 952 cases and 187 840 healthy controls) provided the IHD data. We performed a 2‐sample Mendelian randomization analysis to evaluate the potential causal association between HNRNPC (heterogeneous nuclear ribonucleoprotein C) and IHD, followed by experimental validation in vitro and in vivo to confirm the role of HNRNPC in IHD pathogenesis. Results There was no indication of pleiotropy or heterogeneity among the 6 m6A‐associated proteins, but Mendelian randomization analysis revealed that HNRNPC (odds ratio [OR], 0.93 [95% CI, 0.88–0.97]; P=0.002) was associated with IHD. When IHD developed, there was a significant upregulation of HNRNPC expression in both animal and cellular tests. HNRNPC knockdown prevented oxidative stress, mitochondrial dysfunction, and cell death. Conclusions The Mendelian randomization study suggests a potential causal association of the m6A‐related protein HNRNPC in the cause of IHD and verified the accuracy of the results through a series of experiments, which will help us understand the pathogenesis of IHD and identify potential therapeutic targets in the future.

Type 2 myocardial infarction (T2MI), caused by a mismatch in myocardial oxygen supply and demand, is a common complication in sepsis patients. However, its diagnosis remains challenging due to non-specific clinical presentations and the difficulty in distinguishing it from other causes of troponin elevation. This diagnostic ambiguity creates an urgent need for reliable diagnostic tools, especially since the management of T2MI fundamentally differs from that of type 1 MI. To develop, validate, and evaluate a diagnostic model for type 2 myocardial infarction in sepsis patients. Model development and internal validation were conducted using data from sepsis patients in the Medical Information Mart for Intensive Care IV database. External validation was performed on the intensive care unit patients of Jiading District Central Hospital Affiliated Shanghai University of Medicine & Health Sciences. Variables were selected using backward elimination. Then, they were incorporated into a logistic regression model to construct the diagnostic score. Discriminative ability and calibration were evaluated by the area under the receiver operating characteristic curve and calibration curves, respectively; prediction results were displayed using a nomogram and forest plots. The derivation cohort included 2,519 patients and was divided into a training set (n=1,763) and a test set (n=756). External validation was performed on a separate cohort of 70 patients. Multivariate logistic regression identified the following independent factors associated with T2MI: diabetes mellitus, coronary heart disease, respiratory failure, old myocardial infarction, acute respiratory distress syndrome, septic shock, invasive mechanical ventilation, blood urea nitrogen, prothrombin time, international normalized ratio, temperature, and age. The final model achieved an AUC of 0.81 (95% CI: 0.79–0.83) in the training set, 0.79 (95% CI: 0.76–0.83) in the test set, and 0.78 (95% CI: 0.65–0.91) in the external validation cohort. The calibration curves showed excellent agreement between the predicted and observed probabilities across all datasets, indicating good model calibration. Sensitivity, specificity, positive predictive value, and negative predictive value were consistently high across all datasets. The developed T2MI diagnostic scoring system for sepsis patients demonstrated strong discrimination and calibration, accurately predicting T2MI risk and proving useful for clinical diagnosis. none

Rheumatoid arthritis (RA) with anti-citrullinated protein/peptide antibodies (ACPA + RA) demonstrates more significant radiographic damage compared to ACPA-negative RA (ACPA- RA). Chemokine-activated signaling pathways contribute to the regulation of the bone formation and resorption. The potential role of C-X-C motif chemokine ligand 7 (CXCL7) in bone erosion and its viability as a therapeutic target for RA merit further investigation. Plasma CXCL7 concentration was quantified using enzyme-linked immunosorbent assay (ELISA). The effect of CXCL7 on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogeneis was assessed through tartrate-resistant acid phosphates (TRAP) staining and F-actin ring immunofluorescence. Western blotting analysis was used to identify the signaling pathways activated by CXCL7. To investigate the potential therapeutic effect by targeting Cxcl7, Cxcl7 neutralizing antibodies were administrated intraperitoneally to mice with collagen-induced arthritis (CIA). Histopathology and micro-computed tomography (micro-CT) scanning were utilized to assess joint inflammation and bone destruction in CIA mice. The plasma CXCL7 concentration was significantly higher in ACPA + RA compared with ACPA- RA and healthy controls. The level of CXCL7 was positively correlated with disease activity and bone erosion in RA patients. It was discovered that CXCL7 promoted RANKL-induced osteoclastogenesis in CD14 + monocytes derived from RA patients. Mechanistically, the addition of Cxcl7 significantly enhanced RANKL-induced phosphorylation of ERK1/2 and NFATc1 expresssion. Cxcl7 neutralizing antibody alleviated arthritis severity in CIA by reducing the inflammatory response, osteoclasts numbers, and bone destruction in CIA mice joints. CXCL7 contributes to the bone erosion in RA by enhancing RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathways. CXCL7 could potentially be targeted for therapeutic interventions in RA.

The regeneration and repair of natural bone is a complex and multifaceted process. Potentially, multifunctional scaffolds that exhibit synergistic effects of various biological activities and align with the dynamic bone healing process, are highly expected to achieve desirable bone repairing outcomes. Bioavailable magnesium (Mg) is an essential element taking part in bone regeneration via promoting angiogenesis and osteogenesis. Polyphenol gallic acid (GA) is an anti-inflammatory molecule that can modulate immune microenvironment. To control their release behaviors, Mg2+ and GA can react with each other to form metal-organic frameworks (MOF), which are then embedded into conductive porous scaffolds made of gelatin cryogel and poly(3,4-ethyldioxyethiophene): polystyrene sulfonate (PEDOT:PSS). In in vitro cell culture, the MOF-integrated conductive scaffold can simultaneously provide sustained supply of Mg2+ and GA to modulate the biological responses of a variety of cells. In in vivo evaluations, it shows remarkably enhanced new bone formation, as compared to groups of only MOF-contained non-conductive scaffold or conductive scaffold without MOF in rat calvarial defect model. In summary, conductive scaffold associated with sustained release of bioactive factors can serve as an effective treatment for inducing neo-bone growth benefiting from the synergistical contributions of diverse bioactive factors.

Bariatric surgery presents a significant alleviation for non-alcoholic fatty liver disease (NAFLD), which relies in part on achieving substantial weight loss in post-surgical period. We aimed to understand the effect of bariatric surgery on NAFLD remission via metabolomics and to validate the results in a general population-based cohort. In a pilot study, ten patients with NAFLD who underwent bariatric surgery were enrolled. The remission of hepatic steatosis was assessed by MRI-derived proton density fat fraction (PDFF) before and 3-month after surgery. Temporal associations of body mass index (BMI) reduction, alteration in metabolomic biomarkers, and NAFLD remission were quantified by using cross-lagged models, which were then validated in a general population-based cohort (n = 1258). At 3-month after surgery, BMI reduction of 6.9 (SD 1.9) kg/m2 and MRI-PDFF reduction of 9.6

11554 Background: At the 2024 ASCO conference, we reported preliminary results on the efficacy and safety of IBI110 (anti-LAG-3 antibody) combined with sintilimab (anti-PD-1 antibody) in advanced alveolar soft part sarcoma (ASPS), which demonstrated an overall response rate (ORR) of 48.1%, including three complete responses (CRs). Here, we provide updated results from this single-arm, phase II trial. Methods: Eligible patients with metastatic or unresectable ASPS were assigned to two cohorts: cohort A (immune checkpoint inhibitor [ICI]-naïve, defined as no prior exposure to anti-PD-1/PD-L1/CTLA-4 antibodies) and cohort B (ICI-failed, defined as imaging-confirmed progression following anti-PD-1/PD-L1 therapy). Patients received IBI110 (200 mg) plus sintilimab (200 mg) intravenously every three weeks (Q3W). Primary endpoints were ORR and progression-free survival (PFS), assessed by investigators per RECIST v1.1, as well as safety. Secondary endpoints included overall survival (OS) and safety profile. Results: A total of 28 patients were enrolled (57.1% male; median age: 30.5 years; ECOG performance status 0: 100%; stage IV: 100%), with 20 patients in cohort A and 8 in cohort B. Responses were evaluable in 27 patients. The ORR was 51.8% across the entire population, including 4 CRs and 8 partial responses (PRs) in cohort A, and 2 PRs in cohort B. As of January 8, 2025, the median follow-up duration was 21.3 months (95% CI: 11.5–29.8). Median PFS and OS were not reached in the overall population (see Table). Treatment-related adverse events (TRAEs) occurred in all patients, with grade ≥3 TRAEs observed in 10 (35.7%) patients. Four TRAEs led to treatment discontinuation, including hemoptysis (n=2), type 1 diabetes mellitus (n=1), and encephalitis (n=1). No TRAE-related deaths were reported. Following discontinuation of LAG-3 antibody production in July 2024, patients achieving CR were advised to discontinue therapy, while those with PR or stable disease (SD) transitioned to sintilimab monotherapy. Notably, no disease progression was observed among these patients, including two who were previously resistant to sintilimab. Tumor microenvironment analysis in 17 patients (10 responders and 7 non-responders) revealed significantly higher LAG-3 density in responders compared to non-responders ( P =0.021). Conclusions: The combination of IBI110 and sintilimab demonstrated promising efficacy in both ICI-naïve and ICI-failed advanced ASPS with an acceptable safety profile. The durable restoration of ICI efficacy persisted despite the discontinuation of combination therapy. LAG-3 expression may serve as a predictive biomarker for response to anti-LAG-3 therapy in ASPS. Survival analysis. Cohort PFS (m) OS (m) A Not reached Not reached B 14.9 25.4 Whole population Not reached Not reached PFS: progression-free survival; OS: overall survival.

Background:Renal fibrosis, characterized by the abnormal accumulation of extracellular matrix in renal tissue and progressive loss of kidney function, is posing a significant challenge in clinical treatment. While several therapeutic options exist, effective treatments remain limited. Inonotus obliquus (Chaga), a traditional medicinal mushroom, has shown promising effects in chronic kidney disease (CKD), yet its cellular and molecular mechanisms remain largely unexplored. Methods:We analysed the chemical composition of Chaga using UPLC-MS and predicted its biological targets using PubChem and Swiss Target Prediction. We used single-cell RNA sequencing to study cellular responses in a mouse model of folic acid-induced renal fibrosis, complemented by spatial transcriptomics to map cellular location patterns. Histological assessment was performed using H&E and Masson trichrome staining. Results:For the first time, we employed single-cell RNA sequencing technology to investigate Chaga treatment in renal fibrosis. Histological analysis revealed that Chaga treatment significantly reduced renal tubular damage scores [from 5.00 (5.00, 5.00) to 2.00 (2.00, 2.00), p < 0.05] and decreased collagen deposition area (from 11.40% ± 3.01% to 4.06% ± 0.45%, p < 0.05) at day 14. Through analysis of 82,496 kidney cells, we identified 30 distinct cell clusters classified into eight cell types. Key findings include the downregulation of pro-inflammatory M1 macrophages and upregulation of anti-inflammatory M2 macrophages, alongside decreased T cell responses. Single-cell sequencing revealed differential gene expression in proximal tubular subpopulations associated with reduced fibrosis. Pathway and network pharmacology analyses of 60 identified compounds in Chaga and their 675 predicted targets suggested potential effects on immune and fibrotic pathways, particularly affecting Tregs and NKT cells. Cell-to-cell communication analyses revealed potential interactions between proximal tubular cells, macrophages, and T Cells, providing insights into possible mechanisms by which Chaga may ameliorate renal fibrosis. Conclusion:Our study provided new insights into the potential therapeutic effects of Chaga in renal fibrosis through single-cell sequencing analysis. Our findings suggest that Chaga may represent a promising candidate for renal fibrosis treatment, though further experimental validation is needed to establish its clinical application.

Aim or purpose: This study investigates the mechanotransductive role of Piezo1 in fibrocartilage stem cells (FCSCs) during temporomandibular joint (TMJ) development and osteoarthritis pathogenesis, addressing a critical gap in understanding how mechanical cues regulate craniofacial morphogenesis and disease progression. Materials and methods: We performed single-cell RNA sequencing (scRNA-seq) on human TMJ samples to assess the expression of mechanosensitive ion channels. Conditional knockout mice were generated to study the effects of Piezo1 on condylar development and homeostasis. Specifically, Gli1-CreERT2; Piezo1 fl/fl mice were used to delete Piezo1 in Gli1+ cells. To model TMJOA, unilateral partial discectomy (UPD) was performed, followed by comprehensive analyses including histology and immunohistochemistry to evaluate the impact of Piezo1 deletion. Results: ScRNA-seq revealed prominent PIEZO1 expression in human condylar cartilage and bone, with Piezo1-tdTomato reporter mice confirming its age-independent expression pattern in murine condyles. Conditional Piezo1 knockout in Gli1+ cells disrupted condylar development and homeostasis by impairing fibrocartilage stem cell differentiation, while Piezo1 deletion in a TMJ osteoarthritis model alleviated pathological symptoms, improved condylar morphology, and reduced cartilage degradation through mechanotransduction modulation. Conclusions: Our findings suggest that Piezo1 serves as a critical mechanosensitive regulator enabling Gli1+ FCSCs to perceive physiological mechanical cues and sustain their differentiation capacity into chondrocytes. Deletion of Piezo1 in a physiological context impairs FCSCs differentiation, while in a pathological state it offers protection against TMJOA-induced damage to the condyle by preventing Gli1+ cells depletion.

Diabetic cardiomyopathy (DCM) is a major cause of mortality in patients with diabetes, particularly those with type 2 diabetes. Ferroptosis is closely linked to the onset and progression of various cardiovascular diseases. Irisin, a myokine produced by exercising skeletal muscle, has been shown to mitigate DCM. However, whether irisin alleviates type 2 DCM by inhibiting ferroptosis remains unclear. This study aimed to determine whether irisin prevents DCM by suppressing ferroptosis. First, ferroptosis was examined in palmitic acid (PA)-induced cardiomyocytes. Next, the effects of irisin on PA-induced cardiomyocytes were evaluated. Finally, the molecular mechanisms underlying irisin's protective effects against DCM were investigated. Ferroptosis was identified in an In Vitro model of type 2 DCM induced by PA. Irisin reduced PA-induced ferroptosis and alleviated myocardial injury, as indicated by decreased reactive oxygen species (ROS) production, Fe²⁺ content, and malondialdehyde (MDA) levels, along with increased glutathione (GSH) levels and mitochondrial membrane potential (MMP). Further analysis suggested that irisin does not mitigate PA-induced ferroptosis through iron metabolism or lipid peroxidation pathways but instead inhibits ferroptosis via the System Xc-/GSH/GPX4 axis. Additionally, irisin reduced the secretion of inflammatory cytokines, including IL-1β and IL-6. These findings indicate that irisin prevents the progression of DCM by suppressing ferroptosis through the System Xc-/GSH/GPX4 axis and reducing inflammation.

BackgroundCurrently, pathophysiological mechanisms of post-acute sequelae of coronavirus disease-19-cardiovascular syndrome (PASC-CVS) remain unknown.Methods and resultsPatients with PASC-CVS exhibited significantly higher circulating levels of severe acute respiratory syndrome-coronavirus-2 spike protein S1 than the non-PASC-CVS patients and healthy controls. Moreover, individuals with high plasma spike protein S1 concentrations exhibited elevated heart rates and normalized low frequency, suggesting cardiac beta-adrenergic receptor (beta-AR) hyperactivity. Microscale thermophoresis (MST) assay revealed that the spike protein bound to beta 1- and beta 2-AR, but not to D1-dopamine receptor. These interactions were blocked by beta 1- and beta 2-AR blockers. Molecular docking and MST assay of beta-AR mutants revealed that the spike protein interacted with the extracellular loop 2 of both beta-ARs. In cardiomyocytes, spike protein dose-dependently increased the cyclic adenosine monophosphate production with or without epinephrine, indicating its allosteric effects on beta-ARs.ConclusionSevere acute respiratory syndrome-coronavirus-2 spike proteins act as an allosteric beta-AR agonist, leading to cardiac beta-AR hyperactivity, thus contributing to PASC-CVS.

>Arrhythmogenic cardiomyopathy（ACM）, also known as hereditary cardiomyopathy, is characterized by a gradual loss of cardiomyocytes, which are replaced by fibrous or fibrofatty tissues. The disease was initially designated as arrhythmogenic right ventricular cardiomyopathy, which predisposed to fatal ventricular arrhythmias and sudden cardiac death. [1,2] However, recent insights in autopsy investigations, genotype–phenotype correlation studies,and myocardial tissue characterization by cardiac magnetic resonance（CMR） have broadened our understanding of the disease, revealing that it frequently involves the left ventricle（LV）. [3-5]

TLS area and count in ASPS patients

Afferent baroreflex failure (ABF) is a rare disease. It refers to the clinical syndrome caused by the impairment of the afferent limb of the baroreflex or its central connections at the level of the medulla. The recognized causes include trauma, surgery in related areas (radical neck tumor surgery, carotid endarterectomy), neck radiotherapy, brain stem stroke, tumor growth paraganglioma and hereditary diseases, among which the most common cause is extensive neck surgery or radiotherapy for neck cancer. The main manifestations are fluctuating hypertension, orthostatic hypotension, paroxysmal tachycardia and bradycardia. This case is a young man, whose main feature is blood pressure fluctuation, accom-panied by neurogenic orthostatic hypotension (nOH). After examination, the common causes of hypertension and nOH were ruled out. Combined with the previous neck radiotherapy and neck lymph node dissection, it was considered that the blood pressure regulation was abnormal due to the damage of carotid sinus baroreceptor after radiotherapy for nasopharyngeal carcinoma and neck lymph node dissection, which was called ABF. At the same time, the patient was complicated with chronic hyponatremia. Combined with clinical and laboratory examination, the final consideration was caused by syndrome of in- appropriate antidiuretic hormone (SIADH). Baroreceptors controlled the secretion of heart rate, blood pressure and antidiuretic hormone through the mandatory "inhibition" signal. We speculate that the carotid sinus baroreceptor was damaged after neck radiotherapy and surgery, which leads to abnormal blood pressure regulation and nOH, while the function of inhibiting ADH secretion was weakened, resulting in higher ADH than normal level and mild hyponatremia. The goal of treating ABF patients was to reduce the frequency and amplitude of sudden changes in blood pressure and heart rate, and to alleviate the onset of symptomatic hypotension. At present, drug treatment is still controversial, and non-drug treatment may alleviate some patients' symptoms, but long-term effective treatment still needs further study. The incidence of ABF is not high, but it may lead to serious cardiovascular and cerebrovascular events, and the mechanism involved is extremely complicated, and there are few related studies. The reports of relevant medical records warn that patients undergoing neck radiotherapy or surgery should minimize the da-mage to the baroreceptor in the carotid sinus in order to reduce the adverse prognosis caused by complications.

Erdheim-Chester Disease (ECD) is a rare form of histiocytosis characterized by xanthomatous infiltration of affected organs. We present a case of a 62-year-old man with ECD initially presenting with constrictive pericarditis. Comprehensive imaging revealed systemic involvement, including the skeleton, orbit, pituitary, lung, kidney, and retroperitoneum, despite the absence of related symptoms. The diagnosis of ECD was eventually confirmed through histopathological evidence from a CT-guided biopsy. The patient responded well to interferon-α2b treatment, with gradual symptom amelioration and improvement in imaging and laboratory findings over a 5-month follow-up period. This case highlights the importance of considering ECD in the differential diagnosis of constrictive pericarditis and the utility of multimodal imaging for accurate diagnosis and management of this rare disease. The patient's positive response to treatment also highlights the potential for effective management of ECD, particularly with early diagnosis and intervention.

Cardiovascular diseases are caused by pathological cardiac remodeling, which involves fibrosis, inflammation and cell dysfunction. This includes autophagy, apoptosis, oxidative stress, mitochondrial dysfunction, changes in energy metabolism, angiogenesis and dysregulation of signaling pathways. These changes in heart structure and/or function ultimately result in heart failure. In an effort to prevent this, multiple cardiovascular outcome trials have demonstrated the cardiac benefits of sodium‑glucose cotransporter type 2 inhibitors (SGLT2is), hypoglycemic drugs initially designed to treat type 2 diabetes mellitus. SGLT2is include empagliflozin and dapagliflozin, which are listed as guideline drugs in the 2021 European Guidelines for Heart Failure and the 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America Guidelines for Heart Failure Management. In recent years, multiple studies using animal models have explored the mechanisms by which SGLT2is prevent cardiac remodeling. This article reviews the role of SGLT2is in cardiac remodeling induced by different etiologies to provide a guideline for further evaluation of the mechanisms underlying the inhibition of pathological cardiac remodeling by SGLT2is, as well as the development of novel drug targets.

[This corrects the article DOI: 10.3389/fphar.2021.781640.].