bluuebunny/crossref_metadata_2025_split huggingface dataset:
286-OR: JNK3—A Key Downstream Target of Incretin Responses in ß-Cells
Authors: ANDRADE LOUZADA NETO RUY , GONZALEZ MAREL , PITA-GRISANTI VALENTINA , BLANDINO-ROSANO MANUEL , BERNAL-MIZRACHI ERNESTO 
Published: June 2024

The c-Jun N-terminal Kinases (JNKs) regulate crucial physiological processes. JNK1 and JNK2 exhibit broad tissue distribution and are implicated in insulin resistance, inflammation, and cell signaling. Conversely, JNK3 (MAPK10) is predominantly found in CNS neurons and pancreatic β- cells and the physiological function of this JNK member is less understood. To explore JNK3's role in pancreatic β-cells, we generated mice with JNK3 deletion in beta-cells (βJNK3KO). βJNK3KO exhibited glucose intolerance and insulin secretion only after oral, suggesting a role for JNK3 in incretin responses. Assessment of incretin responses demonstrated impaired insulin secretion induced by Exendin 4 (Ex4) in βJNK3KO and this was associated with reduced GLP1R expression. These findings were validated in human islets treated with a specific JNK3 inhibitor (iJNK3). Downstream of GLP1-R, CREB phosphorylation upon Ex4 was decreased in βJNK3KO islets suggesting a crosstalk between JNK3 and GLP1-R signaling on regulation of acute insulin secretion by incretins. Notably, GLP1R/cAMP/CREB axis induction of IRS2 expression, a master regulator of β-cell survival and growth, was also downregulated in βJNK3KO mice and human islets treated with iJNK3. As a result of decreased IRS2 expression, the protective effect of Ex4 was lost in βJNK3KO islets exposed to proinflammatory cytokines and human islets treated with iJNK3. Finally, the beneficial protective effect of Ex4 treatment was partially attenuated in βJNK3KO in a model of multiple low doses of STZ.
In conclusion, our data identify JNK3 as a novel player in β-cell function and survival and suggest that JNK3 presents a potential therapeutic alternative for incretin-based therapy.

Disclosure
R. Andrade Louzada Neto: None. M. Gonzalez: None. V. Pita-Grisanti: None. M. Blandino-Rosano: None. E. Bernal-Mizrachi: None.

Funding
Grants R01-DK073716, DK132103 and DK133183
295-OR: The PNPLA3 G-allele Reduces the Beneficial Effects of a Healthy Diet on Hepatic Lipid Content in Type 2 Diabetes
Authors: PAFILI KALLIOPI , ZAHARIA OANA P. , STRASSBURGER KLAUS , KNEBEL BIRGIT , HERDER CHRISTIAN , HUTTASCH MAXIMILIAN , KARUSHEVA YANISLAVA , KABISCH STEFAN , STROM ALEXANDER , SZENDROEDI JULIA , RODEN MICHAEL 
Published: June 2024

Introduction & Objective: Weight loss is pivotal for, but variably effective in type 2 diabetes (T2D) and comorbidities. The G-allele in the rs738409 single nucleotide polymorphism within the patatin-like phospholipase domain-containing protein 3 (PNPLA3) associates with liver steatosis and differently with insulin resistance. We hypothesized that this G-allele may affect response to dietary interventions.
Methods: T2D volunteers (age 18-69 years, BMI ≥30 kg/m2, HbA1c &lt;9.0%) were randomly assigned to 8-w hypocaloric diets (1.256 kJ reduction in total daily energy intake), either high in cereal fiber and coffee, but red meat-free (healthy diet [HD]; n=16), or low in fiber, devoid of coffee, but rich in red meat (unhealthy diet [UD]; n=15). Genotyping was performed for the PNPLA3 gene. Insulin sensitivity (M-value) was measured by hyperinsulinemic-euglycemic clamps, hepatic lipid content (HCL) by 1H magnetic resonance spectroscopy before and after the intervention.
Results: Baseline HCL was similar between groups (carriers: UD 18.5±8.5%, HD 14.6±8.4%; non-carriers: UD 13.5±4.2%, HD 17.8±7.3%). In the face of comparable body weight reduction (~4.7%), carriers and non-carriers decreased HCL from 0 to 8 weeks of UD (-57% and -46%, p&lt;0.05), with no difference between groups. HD also led to reduction in HCL in non-carriers, but to lesser extent in carriers (-65% vs. -36%, p&lt;0.05 vs baseline and between groups). Changes from baseline in liver fibrosis markers (fibrosis-4 index, AST/platelet ratio index, Forns score) and inflammation (interleukins) did not differ by carrier status. M-value improved in all groups (carriers +27% and non-carriers +21% on HD and carriers on UD +37%, all p&lt;0.05 vs baseline) except for the non-carriers on UD.
Conclusion: Low-energy diets improve insulin sensitivity and steatosis in T2D but the presence of the G allele of PNPLA3 reduces the beneficial effects of a healthy (cereal- and coffee-enriched, but red meat-free) diet on liver lipid content.

Disclosure
K. Pafili: None. O.P. Zaharia: None. K. Strassburger: None. B. Knebel: None. C. Herder: None. M. Huttasch: None. Y. Karusheva: None. S. Kabisch: Other Relationship; Sanofi, Boehringer-Ingelheim, Berlin-Chemie AG. Research Support; J. Rettenmaier & Söhne, Rosenberg, Germany, California Walnut Commission, Almond Board of California, Wilhelm-Doerenkamp-Foundation. Other Relationship; JuZo-Akademie, Lilly Diabetes. A. Strom: Consultant; Wörwag Pharma. J. Szendroedi: None. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer-Ingelheim. Advisory Panel; Novo Nordisk. Research Support; Novo Nordisk. Advisory Panel; TARGET PharmaSolutions, Inc. Speaker's Bureau; AstraZeneca.
300-OR: Beneficial Effect of the Combination Therapy of Cagrilintide, a Dual Amylin/Calcitonin Agonist, and Tirzepatide, a Dual GLP-1/GIP Agonist, on Body Weight Loss in Obese Rats
Authors: VALDECANTOS PILAR , RADA PATRICIA , GHOSH SOUMITRA , RONDINONE CRISTINA M. , VALVERDE ANGELA M. 
Published: June 2024

Introduction & Objective: Combinatorial therapies with incretin receptor agonists targeting multiple pathways that regulate energy balance is a promising strategy for weight loss since it potentially allows dose reduction of each drug and can help to ameliorate the associated gastrointestinal side-effects of the current monotherapies. We evaluated the combination of cagrilintide and tirzepatide on weight loss in obese rats.
Methods: Diet-induced obese Sprague Dawley male rats were dosed subcutaneously once-daily for 12 days with 3 and 10 nmol/kg of cagrilintide and tirzepatide alone or in combination at submaximal dose of 3 nmol/kg. Body weight and food intake were measured daily. Biochemical parameters in plasma were analyzed.
Results: Relative to vehicle, cagrilintide administered alone presented superior efficacy in body weight reduction (-7.22%±1.80% at 3 nmol/kg and -9.61% ± 0.52% at 10 nmol/kg) compared with tirzepatide (-2.53% ± 0.44% at 3 nmol/kg and -5.81 ± 0.86% at 10 nmol/kg). Peptide combination at submaximal dose of 3 nmol/kg each reduced body weight by -11.0 ± 0.86% (P&lt;0.05 vs cagrilintide and P&lt;0.001 versus tirzepatide) at the same doses, Reductions in cumulative food intake correlated with weight loss. Combination therapy was superior in decreasing ALT than cagrilintide (P&lt;0.001) and tirzepatide (P&lt;0.05) and plasma TGs levels were lower compared to the tirzepatide group (P&lt; 0.001).
Conclusion: Combination therapy at submaximal doses of cagrilintide and tirzepatide achieved significantly greater weight loss and higher reduction in food intake compared to the monotherapy, suggesting the potential opportunity of this combination for further clinical development.

Disclosure
P. Valdecantos: Research Support; Pep2Tango Therapeutics INC. P. Rada: Research Support; Pep2Tango Therapeutics INC. S. Ghosh: Consultant; Abvance Therapeutics, Akero Therapeutics, Inc., Fractyl Health, Inc., Takeda Pharmaceutical Company Limited. C.M. Rondinone: Board Member; Pep2tango Therapeutics Inc. Stock/Shareholder; Pep2tango Therapeutics Inc. A.M. Valverde: Research Support; Pep2Tango Therapeutics INC.

Funding
Pep2Tango Therapeutics INC
301-OR: Synergistic Effects of Dapagliflozin and Tirzepatide Combination Treatment on Weight Loss and Glucose Regulation in Diet-Induced Obese Animals
Authors: ABU-FARHA MOHAMED , AL-KHAIRI IRINA , QADDOUMI MOHAMMAD , ALAJMI FAHAD , ABUKHALAF NERMEEN A. , CHERIAN PREETHI T. , AREFANIAN HOSSEIN , ABUBAKER JEHAD , ABDUL-GHANI MUHAMMAD , AL-MULLA FAHD 
Published: June 2024

Background: Tirzepatide is a dual GLP-1 and GIP receptor agonist that enhances glucose-stimulated insulin secretion and significantly lowers HbA1c as well as weight. SGLT2 has also been shown to reduce weight in addition to their glucose lowering effect. Given their different modes of action we hypothesized that their combination would produce additive improvements in weight loss as well as their glycemic control.
Methods: A total of 40 male Sprague Dawley rats aged 6-8 weeks were fed a Normal Diet or high-fat cafeteria diet for 12 weeks. Animals on high fat diet were then divided into four groups treated with either placebo, 100 nmole/kg Tirzepatide, Dapagliflozin 1mg/kg or a combination of Dapagliflozin and Tirzepatide for 6 weeks. Weight, FBG, and calorie consumption were monitored on a weekly basis. The study concluded with the administration of OGTT and ITT tests, followed by the collection of various tissues.
Results: After treatment, animals on normal diet weight of 522.9±11.7g, placebo-treated obese animals were 671.3 ± 26.2g, compared to 598.9 ± 23.4g in dapagliflozin-treated, 532.3±23.0g in Tirzepatide-treated animals, and 480.7± 18.8 g in animals treated with the combination (p&lt;0.001). The addition of dapagliflozin to Tirzepatide resulted in a significant additive improvement in glucose AUC compared to Tirzepatide alone. Moreover, omental, and subcutaneous adipose tissue weight was significantly decreased in animals treated with the combination compared to Tirzepatide alone.
Conclusion: The addition of dapagliflozin to tirzepatide resulted in further weight reduction and improvement in glycemic control compared to each drug alone.

Disclosure
M. Abu-Farha: None. I. Al-khairi: None. M. Qaddoumi: None. F. Alajmi: Consultant; Novo Nordisk. Research Support; Novo Nordisk. Speaker's Bureau; Novo Nordisk. N.A. Abukhalaf: None. P.T. Cherian: None. H. Arefanian: None. J. Abubaker: None. M. Abdul-Ghani: None. F. Al-Mulla: None.

Funding
Kuwait Foundation for the Advancement of Sciences
314-OR: A Randomized Study of a GPR119 Agonist on Glucagon Counterregulation during Hypoglycemia in Type 1 Diabetes Mellitus (T1DM)
Authors: BILAL ANIKA , CASU ANNA , YI FANCHAO , MUCINSKI JUSTINE M. , MERCOUFFER GINA , KELLEY DAVID E. , PRATLEY RICHARD E. 
Published: June 2024

Introduction: Activation of GPR119 receptors (expressed on enteroendocrine and pancreatic islet cells) augments glucagon counter-regulatory responses to hypoglycemia in pre-clinical models. This response is studied using MBX-2982, a GPR119 agonist, in participants with T1D.
Methods: This phase 2a double-blind, cross-over study randomized participants (age;20-60 years, T1D diagnosis ≥5 years) to treatment with 600 mg MBX-2982 or placebo for 14 days with two weeks washout between periods. The study endpoints included glucagon response, epinephrine response, and endogenous glucose production during a euglycemic/hypoglycemic clamp. Glucagon, GLP-1, and GIP in response to a mixed meal test and glycemic metrics from continuous glucose monitor (10 days) were also measured.
Results: 18 participants (age 38.3±12 years, 50% females, 88.9% White, A1c 7.0±0.8%) were enrolled. Compared to placebo, MBX-2982 did not alter counter-regulatory responses to insulin-induced hypoglycemia. GLP-1 response to the MMT were higher following MBX-2982 administration. (Table)
Conclusion: GPR119 activation with MBX-2982 did not improve glucagon counterregulatory responses to hypoglycemia in participants with T1D. The significant increases in fasting GLP-1 and responses during the MMT are consistent with GPR119 target engagement and the expected pharmacodynamic response from L-cells.

Disclosure
A. Bilal: None. A. Casu: None. F. Yi: None. J.M. Mucinski: None. G. Mercouffer: None. D.E. Kelley: Consultant; Pramana Pharmaceuticals, Inc. R.E. Pratley: Other Relationship; Bayer AG, Dompé, Endogenex, Inc., Gasherbrum Bio, Inc., Hengrui (USA) Ltd., Intas Pharmaceuticals Ltd., Eli Lilly and Company, Merck Sharp & Dohme Corp., Novo Nordisk, Novo Nordisk, Pfizer Inc., Rivus Pharmaceuticals Inc., Sun Pharmaceutical Industries Ltd. Consultant; AbbVie Inc., AstraZeneca. Other Relationship; Bayer HealthCare Pharmaceuticals, Inc., Biomea Fusion, Carmot Therapeutics, Inc., Corcept Therapeutics, Fractyl Health, Inc., Genprex. Consultant; Getz Pharma. Other Relationship; Lilly USA LLC, Sanofi. Consultant; Scholar Rock, Inc.

Funding
The Helmsley Charitable Trust, CymaBay Therapeutics.
339-OR: Enhanced Expression of Zinc Finger Protein 385D Leads to Type 2 Diabetes Phenotype in Human Beta Cells
Authors: LU GEMING , KANG RANDY , VARELA MIGUEL A. , OH EUNJIN , THURMOND DEBBIE C. , GARCIA-OCANA ADOLFO 
Published: June 2024

Identification of molecular mechanisms that regulate glucose-stimulated insulin secretion (GSIS) and β-cell identity and growth are essential to develop therapeutic approaches to treat diabetes. Zinc finger protein 385D (ZNF385D) is a nuclear protein that belongs to the Krüppel C2H2-type zinc-finger protein family. Gene-Wide Association Studies have strongly associated ZNF385D gene variants with type 2 diabetes (T2D) onset. Using scRNA-seq and snRNA-seq of adult nondiabetic human islets, we have recently reported that the ZNF385D gene is specifically expressed in human β cells, and its expression negatively correlates with INS expression. However, the role of ZNF385D in the human β cell is unknown. Here, we have addressed this point by overexpressing ZNF385D in EndoC-βH1 cells and human islets and analyzed gene expression, GSIS, and β cell survival. Mining of scRNA-seq data from human islets of nondiabetic and T2D donors from HIRN-HPAP showed that ZNF385 expression is significantly enhanced while INS expression is significantly decreased in β-cells of T2D islets. Overexpression of ZNF385D in EndoC-βH1 cells and human islets led to significant downregulation of INS, PDX1, MAFA, SLC2A2, SNAP25 and VAMP2 genes and significant upregulation of T2D β-like genes such as RFX7, PPAR γ, PPAR α, RB1, POU5F1, NANOG and MYCL. ZNF385D overexpression significantly reduced GSIS without altering basal secretion. scRNA-seq analysis of human islets showed a positive correlation between ZNF385D expression and activation of senescence, apoptosis and metabolic inflexibility pathways in β-cells. Indeed, β-cell death was significantly enhanced by ZNF385D overexpression after treatment with cytokines (TNFα, IL1β, and IFNγ) as assessed by flow cytometry and TUNEL staining. Taken together, these studies indicate that enhanced expression of the β-cell specific gene ZNF385D causes detrimental effects in the function, identity and survival of the human β-cell leading to a T2D-like phenotype.

Disclosure
G. Lu: None. R. Kang: None. M.A. Varela: None. E. Oh: None. D.C. Thurmond: Consultant; Truebindings. A. Garcia-Ocana: Consultant; Sun Pharmaceutical Industries Ltd.

Funding
AR-DMRI Innovative Award
34-PUB: Prescription Pattern of SGLT-2 Inhibitors among Seniors with Type 2 Diabetes Mellitus and Chronic Kidney Disease in a Primary Care Setting
Authors: NAOUS ELIE , ELNAJJAR MAYSSAM , ALHADDAD JULIANO , ACHKAR ANGELA , JABER BERTRAND L. , HE ZHIHENG 
Published: June 2024

Background: SGLT-2 inhibitors (SGLT2i) remain under-prescribed in eligible patients with chronic kidney disease (CKD) and type 2 diabetes mellitus (T2DM), despite of its proven efficacy in renal protection. Data in geriatric population lacks.
Methods: As part of a quality improvement project, this baseline cross-sectional evaluation assesses SGLT2i prescription rates in seniors (age ≥65 years old), with T2DM and CKD stages 3-4 (eGFR 20-59 mL/min/1.73 m2) at a primary care clinic (August to November 2023).
Results: Eighty-one eligible patients were included, 56.8% were women. Mean (±SD) age was 81.7 ± 8.2 years old. Mean HbA1c was 7.1 ± 1.2%, and mean eGFR was 42.4 ± 10.9 ml/min/1.73m². Notably, 11% were not screened for proteinuria in the prior year, and 47.2% of screened individuals exhibited proteinuria. As shown in table 1, SGLT2i were prescribed in 40.7% of patients with CKD, but their use was significantly higher among patients with vascular disease (72.7%), heart failure (57.6%), and those requiring insulin (42.4%).
Conclusion: In a primary care clinic, SGLT2i were prescribed in 40.7% of seniors with T2DM and CKD but were commonly used among patients with cardiovascular diseases and those requiring insulin. Further investigation is needed to understand this gap in knowledge and formulate a mitigation strategy to expand SGLT2i use in eligible patients.

Disclosure
E. Naous: None. M. Elnajjar: None. J. Alhaddad: None. A. Achkar: None. B.L. Jaber: Other Relationship; Up-To-Date. Consultant; Avania, LLC (Ad Hoc Member, Clinical Events Committee). Z. He: None.
377-P: Assessing the Counterregulatory Response to Hypoglycemia with Amitriptyline
Authors: MUSIC MEGAN B. , THOMPSON ANDREA , ILES ASHLEY , MARKSBURY ASHLEE R. , PATEL BANSI , SCHOEDER LILY A. , WOOTEN MASON , BECKNER ZACH , DEVORE MICAH H. , MACON ERICA L. , FISHER SIMON J. 
Published: June 2024

Introduction & Objectives: Our laboratory previously demonstrated a beneficial effect of amitriptyline, a serotonin and norepinephrine reuptake inhibitor, in preventing impaired hypoglycemic counterregulation. We wished to extend these findings to a diabetic animal model.
Methods: Streptozotocin (STZ, 65 mg/kg IP) diabetic 10-week-old male Sprague Dawley rats were randomized to 3 groups: STZ+RS (n=7, RS=recurrent saline controls), STZ+RH (n=6, RH=recurrent hypoglycemia), and STZ+AMP+RH (n=8, AMP=amitriptyline 10 mg/kg, IP). After 3-days preconditioning, animals underwent a hyperinsulinemic (50mU/kg/min) hypoglycemic (~45 mg/dL) clamp.
Results: In response to hypoglycemia, peak epinephrine levels were blunted in STZ+RH (299±51 pg/ml) compared to STZ+RS (1084±916, p&lt;0.01 vs STZ+RS), and did not improve significantly in STZ+AMP+RH (482±227, p=NS vs STZ+RH). Similarly, the glucagon response to hypoglycemia demonstrated a blunted response with STZ+AMP+RH (see Figure).
Conclusion: The beneficial effects of amitriptyline in restoring the counterregulatory response to hypoglycemia that were initially observed in nondiabetic model seem to be attenuated in the insulin deficient diabetic rodent model. It is concluded that chronic diabetes abrogates the beneficial effects of serotonin and norepinephrine reuptake inhibitors on the sympathoadrenal and counterregulatory responses to hypoglycemia.

Disclosure
M.B. Music: None. A. Thompson: None. A. Iles: None. A.R. Marksbury: None. B. Patel: None. L.A. Schoeder: None. M. Wooten: None. Z. Beckner: None. M.H. Devore: None. E.L. Macon: None. S.J. Fisher: None.
387-P: Finerenone Attenuates Kidney GLP-1 Receptor Downregulation in Mice with Comorbid Diabetes
Authors: TIN TRAN DUC , HONG LISA Y.Q. , KAUR HARMANDEEP , YEUNG EMILY S.H. , ADVANI SUZANNE L. , LIU YOUAN , NAGARJUN BATCHU SRI , ADVANI ANDREW 
Published: June 2024

Introduction & Objective: Several new treatments have recently been shown to have kidney protective benefits in people with diabetes. Because these treatments were developed in parallel, at the time of their clinical trial participation many individuals were not receiving concurrent treatment with other therapies subsequently also found to have kidney protective benefits. Accordingly, it is unclear whether treatments recently shown to slow kidney function decline will have additive or redundant effects when used in combination. Here, we examined the effects of the mineralocorticoid receptor antagonist finerenone on kidney GLP-1 receptor (GLP-1R) expression levels in mice with comorbid diabetes.
Methods: Mice were fed a high fat diet and received a single intraperitoneal injection of streptozotocin 12 weeks into high fat diet feeding (DM-HFD mice). After 24 weeks, animals were fed high fat diet containing finerenone (100mg/kg diet) for a further 2 weeks. Kidney GLP-1R localization and expression were analyzed by RNAscope in situ hybridization and qRT-PCR.
Results: Blood glucose, HbA1c and systolic blood pressure were unaffected by 2-week treatment of DM-HFD mice with finerenone. GLP-1R mRNA was detectable in vascular smooth muscle cells of kidney arterioles, and also present in juxtaglomerular apparatus cells, being sparse or absent in other kidney cells. Kidney GLP-1R mRNA levels were reduced in DM-HFD mice and this reduction was negated by finerenone (GLP-1R:RPL13A mRNA (fold) control 1.02±0.22, DM-HFD 0.67±0.09 (p&lt;0.05 vs. control), DM-HFD + finerenone 1.10±0.34 (p&lt;0.01 vs. DM-HFD)).
Conclusion: Kidney GLP-1R expression is diminished in aged mice with comorbid diabetes. This reduction is negated by treatment with the mineralocorticoid receptor antagonist finerenone. Both GLP-1R agonism and finerenone have demonstrated kidney protective benefits in people with diabetes. The present findings lend mechanistic support for the additive potential of combination therapy.

Disclosure
D. Tran: None. L.Y.Q. Hong: None. H. Kaur: None. E.S.H. Yeung: None. S.L. Advani: None. Y. Liu: None. S. Batchu: None. A. Advani: None.
392-P: Gemigliptin Attenuates TGF-ß-Induced Renal Fibrosis by Inhibiting the TGF-ß/Smad3 Signaling Pathway through the Upregulation of FGF21 Expression
Authors: JUNG GWONSOO 
Published: June 2024

Aim: Fibroblast growth factor 21 (FGF21), a well-known regulator of metabolic disorders, exhibits the potential to prevent renal fibrosis by negatively regulating the transforming growth factor β (TGF-β)/Smad3 signaling pathway. Gemigliptin, known as a dipeptidyl peptidase-4 inhibitor, is frequently utilized in the management of patients with type 2 diabetes. However, the protective effects of gemigliptin on renal fibrosis, particularly concerning its potential to upregulate the expression of fibroblast growth factor 21, remains incompletely understood. The purpose of this study was to investigate the gemigliptin’s renoprotective effects against TGF-β-induced renal fibrosis by enhancing the expression of fibroblast growth factor 21 in the cultured human proximal tubular epithelial cell line, HK-2.
Methods: HK-2 cells were maintained with keratinocyte-free medium according to the supplier’s recommendations, and exposed to the indicated doses of TGF-β, FGF21, and gemigliptin for 24 h. To elucidate the effect of FGF21, knockdown experiments were conducted by transfecting HK-2 cells with small interfering RNA targeting the fibroblast growth factor 21 for 24 h.
Results: Treatment of FGF21 effectively prevented TGF-β-induced renal fibrosis by attenuating TGF-β/Smad3 signaling pathway. Similarly, Gemigliptin showed protective effects against TGF-β-induced renal fibrosis by mitigating TGF-β/Smad3 signaling, which is achieved through the upregulation of FGF21 expression. However, the protective effects of gemigliptin were blocked when FGF21 expression was knockdowned in TGF-β-treated HK-2 Cells.
Conclusion: These results indicate that gemigliptin has the potential to confer protective effects against TGF-β-induced renal fibrosis by elavating FGF21 expression levels in the cultured human proximal tubular epithelial cells.

Disclosure
G. Jung: None.

Funding
National Research Foundation of Korea (RS-2023-00252005)