The DOI matches its Crossref record; 78 of the 78 references it cites were found in a registry or an index.
Hyperglycemia-Driven Inhibition of AMP-Activated Protein Kinase α2 Induces Diabetic Cardiomyopathy by Promoting Mitochondria-Associated Endoplasmic Reticulum Membranes In Vivo
Open accessAbstract
Background: Fundc1 (FUN14 domain containing 1), an outer mitochondrial membrane protein, is important for mitophagy and mitochondria-associated endoplasmic reticulum membranes (MAMs). The roles of Fundc1 and MAMs in diabetic hearts remain unknown. The aims of this study, therefore, were to determine whether the diabetes mellitus–induced Fundc1 expression could increase MAM formation, and whether disruption of MAM formation improves diabetic cardiac function. Methods: Levels of FUNDC1 were examined in the hearts from diabetic patients and nondiabetic donors. Levels of Fundc1-induced MAMs and mitochondrial and heart function were examined in mouse neonatal cardiomyocytes exposed to high glucose (HG, 30 mmol/L d -glucose for 48 hours), and in streptozotocin-treated cardiac-specific Fundc1 knockout mice and cardiac-specific Fundc1 knockout diabetic Akita mice, as well. Results: FUNDC1 levels were significantly elevated in cardiac tissues from diabetic patients in comparison with those from nondiabetic donors. In cultured mouse neonatal cardiomyocytes, HG conditions increased levels of Fundc1, the inositol 1,4,5-trisphosphate type 2 receptor (Ip 3 r2), and MAMs. Genetic downregulation of either Fundc1 or Ip 3 r2 inhibited MAM formation, reduced endoplasmic reticulum-mitochondrial Ca 2+ flux, and improved mitochondrial function in HG-treated cardiomyocytes. Consistently, adenoviral overexpression of Fundc1 promoted MAM formation, mitochondrial Ca 2+ increase, and mitochondrial dysfunction in cardiomyocytes exposed to normal glucose (5.5 mmol/L d -glucose). In comparison with nondiabetic controls, levels of Fundc1, Ip 3 r2, and MAMs were significantly increased in hearts from streptozotocin-treated mice and Akita mice. Furthermore, in comparison with control hearts, diabetes mellitus markedly increased coimmunoprecipitation of Fundc1 and Ip 3 r2. The binding of Fundc1 to Ip 3 r2 inhibits Ip 3 r2 ubiquitination and proteasome-mediated degradation. Cardiomyocyte-specific Fundc1 deletion ablated diabetes mellitus–induced MAM formation, prevented mitochondrial Ca 2+ increase, mitochondrial fragmentation, and apoptosis with improved mitochondrial functional capacity and cardiac function. In mouse neonatal cardiomyocytes, HG suppressed AMP-activated protein kinase activity. Furthermore, in cardiomyocytes of Prkaa2 knockout mice, expression of Fundc1, MAM formation, and mitochondrial Ca 2+ levels were significantly increased. Finally, adenoviral overexpression of a constitutively active mutant AMP-activated protein kinase ablated HG-induced MAM formation and mitochondrial dysfunction. Conclusions: We conclude that diabetes mellitus suppresses AMP-activated protein kinase, initiating Fundc1-mediated MAM formation, mitochondrial dysfunction, and cardiomyopathy, suggesting that AMP-activated protein kinase–induced Fundc1 suppression is a valid target to treat diabetic cardiomyopathy.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“In addition, AMPK activation reversed DCM by suppressing high glucose-induced MAM formation, mitochondrial Ca2+ increase, and mitochondrial dysfunction in cultured mouse neonatal cardiomyocytes 139].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [139]
In the citing paper
“High glucose-driven inactivation of AMPK increased FUNDC1, resulting in aberrant MAM formation, mitochondrial Ca2+ increase, mitochondrial dysfunction, and cardiac dysfunction [139].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [139]
In the citing paper
“These findings illustrating the results of AMPK activation, likely via downregulation of FUNDC1-related MAMs, represent a new therapeutic avenue for treating DCM [139].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [139]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Biochemistry and molecular cell biology of diabetic complications
Brownlee, M. (2001) · Nature · doi:10.1038/414813a · Cited by 9,107
Down-Regulation of Na+/K+ATPase Activity by Human Parvovirus B19 Capsid Protein VP1
Almilaji, A., Szteyn, K., Fein, E., Pakladok, T., Muñoz, C., Elvira, B., Towhid, S. T., Alesutan, I., Shumilina, E. V., Bock, C. –., et al. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350083 · Cited by 8,700
Role of AMP-Activated Protein Kinase in Mechanism of Metformin Action
Zhou, G., Myers, R., Li, Y., Chen, Y., Shen, X., Fenyk-Melody, J., Wu, M., Ventre, J., Doebber, T., Fujii, N., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci13505 · Cited by 5,652
Cillà, S. D., Farruggio, S., Vujosevic, S., Raina, G., Filippini, D. A., Gatti, V., Clemente, N., Mary, D., Vezzola, D., Casini, G., et al. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000479441 · Cited by 5,154
The Pathophysiology of Mitochondrial Cell Death
Green, D. R., & Kroemer, G. (2004) · Science · doi:10.1126/science.1099320 · Cited by 3,487
Regulation of cell death: the calcium–apoptosis link
Orrenius, S., Zhivotovsky, B., & Nicotera, P. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1150 · Cited by 3,060
Mitofusin 2 tethers endoplasmic reticulum to mitochondria
de Brito, O. M., & Scorrano, L. (2008) · Nature · doi:10.1038/nature07534 · Cited by 2,442
Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes
Kelley, D. E., He, J., Menshikova, E. V., & Ritov, V. B. (2002) · Diabetes · doi:10.2337/diabetes.51.10.2944 · Cited by 2,321
Flagged first, then by citations
Cited by
Sorted by citations
Items 201–300 of 312
Lv, Y., Chen, L., Li, L., Liao, Z., Fang, Z., Cheng, L., & Peng, F. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1535401 · Cited by 9
LncRNA HCG18 affects diabetic cardiomyopathy and its association with miR-9-5p/IGF2R axis
Luo, Y., Jiang, Y., Zhong, T., Li, Z., He, J., Li, X., & Cui, K. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e24604 · Cited by 7
Ding, J., Ji, R., Wang, Z., Jia, Y., Meng, T., Song, X., Gao, J., & He, Q. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1405545 · Cited by 7
Li, Y., Li, H., Shao, J., Zhu, L., Xie, T., Cai, J., Wang, W., Cai, M.-X., Wang, Z., Yao, Y., et al. (2022) · Research Square · doi:10.21203/rs.3.rs-2093332/v1 · Cited by 9
Yang, M., Qin, X., & Liu, X. (2025) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2025.106087 · Cited by 8
Gao, Y., Li, E., Li, F., Cui, Y., Shu, Q., Zhang, Y., Kong, L., Li, H., & Yang, X. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-025-05793-8 · Cited by 7
Zheng, T., Luo, L., Wang, X., Deng, X., & Xue, M. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.112038 · Cited by 8
Wu, X., Yang, J. H., & He, J.-D. (2025) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s541768 · Cited by 7
Yin, X., Wei, Y., Liu, Y., Chen, G. V., Chen, J., Cheng, J., Liu, Y., & Wei, H. (2026) · APOPTOSIS · doi:10.1007/s10495-025-02224-8 · Cited by 6
Investigation of crucial genes and mitochondrial function impairment in diabetic cardiomyopathy
Tuersuntuoheti, M., Zhou, L., Li, J., Yang, S., Zhou, S., & Gong, H. (2024) · Gene · doi:10.1016/j.gene.2024.148563 · Cited by 6
Ren, F., Yang, M., Liu, G., Qi, Y., Li, A., Li, J., & Zheng, L. (2024) · Clinical and Experimental Hypertension · doi:10.1080/10641963.2024.2358030 · Cited by 7
Lu, Y., Fang, Y.-X., Ouyang, Z. M., Wu, T., Zhang, Q., Zou, Y.-W., Zheng, H.-W., Jing, J., Lin, L., Ma, J., et al. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.111829 · Cited by 5
Li, J., Li, D., Zhao, F., Wang, Y., Yao, H., Wu, Y., An, J., Liu, Z., Ding, Y., & Zou, M. (2026) · Nature Communications · doi:10.1038/s41467-026-68548-4 · Cited by 5
Pathological implications of cellular stress in cardiovascular diseases
Ulaganathan, T., Perales, S. G., Mani, S., Baskhairoun, B. A., & Rajasingh, J. (2023) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2023.106397 · Cited by 6
Li, X., Liu, L., Lou, H., Dong, X., Hao, S., Sun, Z., Dou, Z., Li, H., Zhao, W., Sun, X., et al. (2025) · Frontiers of Medicine · doi:10.1007/s11684-024-1102-6 · Cited by 5
Progress in the mechanism of mitochondrial dysfunction in septic cardiomyopathy
Yin, L., Tang, Y., Lin, X., & Jiang, B. (2022) · All Life · doi:10.1080/26895293.2022.2156622 · Cited by 5
TRPV1 in Cardiovascular Disease: A Molecular Nexus of Treatment
Lu, Q., Ding, X., & Gao, B. (2026) · Biomolecules · doi:10.3390/biom16030344 · Cited by 4
Sun, L., Wei, S., Wang, C., Zhang, Y., Zan, X., Li, L., & Zhang, C. (2024) · Materials Today Bio · doi:10.1016/j.mtbio.2024.101310 · Cited by 4
Nuciferine alleviates non-alcoholic steatohepatitis by restoring endoplasmic reticulum stress
Zhao, Z., Zong, Y., Zhang, W., Wang, K., Yang, Y., & Li, F. (2025) · Experimental Cell Research · doi:10.1016/j.yexcr.2025.114599 · Cited by 5
Dai, L., Wang, M., Wang, B., Liang, H., Yang, G., Du, Z., & Wang, H. (2025) · Frontiers in Nutrition · doi:10.3389/fnut.2025.1634555 · Cited by 4
Huang, B., Yulin, Y., Liu, J., Zhang, B., & Lin, N. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1533007 · Cited by 4
Gong, X., Yu, Z., Huang, Z., Xie, L., Zhou, N., Wang, J., Liang, Y., Qin, S., Nie, Z., Wei, L., et al. (2020) · Journal of Interventional Cardiac Electrophysiology · doi:10.1007/s10840-020-00768-0 · Cited by 5
Expression of farnesyl pyrophosphate synthase is increased in diabetic cardiomyopathy
Li, Z., Zhang, J., Wang, M., Qiu, F., Jin, C., & Fu, G. (2021) · Cell Biology International · doi:10.1002/cbin.11573 · Cited by 4
Liu, Q., Meng, F.-L., Du, J., Li, W., Zhou, S., & Li, Y. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.112170 · Cited by 4
FUNDC1 deficiency aggravates endothelial senescence and retinal dysfunction
Ning, J., Li, Z., Mu, Y., Li, X., Li, K., Xing, W., & Zhang, H. (2025) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2025.168093 · Cited by 3
Ablation of mitochondrial calcium uniporter alleviates cardiac dysfunction in type 1 diabetes
Deb, A., Gomez, V., Cheng, Y., Li, Z., Yang, J., Dowllah, I. M., Nguyen, N., Adekanye, O., Smuder, A. J., Cheng, Z., et al. (2025) · Cell Calcium · doi:10.1016/j.ceca.2025.103106 · Cited by 3
Han, H.-L., Zhang, L.-M., Wang, Z.-C., Zhang, H., Wang, J., Du, H.-B., Cui, J.-L., Zhang, G., Niu, C., & Zhao, Z.-G. (2026) · Journal of Nutrition · doi:10.1016/j.tjnut.2026.101589 · Cited by 3
Tang, H., Wang, J., Ji, G., Yang, X., Yang, H., Chen, X., Yang, X., Zhao, H., & He, X. (2024) · Applied Biochemistry and Biotechnology · doi:10.1007/s12010-024-05113-z · Cited by 3
Molecular and biological approach to ischemia/reperfusion in diabetes conditions
Kilic, M., & Halıcı, Z. (2025) · Molecular Biology Reports · doi:10.1007/s11033-025-10686-x · Cited by 3
Zhang, S., Su, B., Wang, L., Tang, S., & Chen, G. (2022) · PubMed Central · doi:10.12122/j.issn.1673-4254.2022.12.14 · Cited by 3
Lymbouris, M., Gooday, C., & Dhatariya, K. (2019) · Medical Hypotheses · doi:10.1016/j.mehy.2019.109439 · Cited by 3
Kandasamy, J., Li, R., Vamesu, B. M., Olave, N. C., Halloran, B., Jilling, T., Ballinger, S. W., & Ambalavanan, N. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.05.17.541177 · Cited by 3
Wu, C., Wei, M. A., Li, A., Zhu, Q., Guo, J., Sun, A., Gu, X., Li, Y., & 宫雁冰 (2026) · Biomedicines · doi:10.3390/biomedicines14071427 · Cited by 2
Wu, Q. E., Yu, S., & Peng, K. (2023) · Critical Reviews in Immunology · doi:10.1615/critrevimmunol.2023050364 · Cited by 2
Zhang, Z., Wang, Y., Zhou, F., Xu, S., Zhang, X., Yue-ying, M., Liu, Y., & He, Y. (2024) · Journal of Food Biochemistry · doi:10.1155/2024/2602406 · Cited by 2
Zhu, L., Zhang, J., Fan, W., Su, C., & Jin, Z. (2024) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2024.1409605 · Cited by 2
IP6K1 Rewires LKB1 Signaling to Mediate Hyperglycemic Endothelial Senescence
Xing, C., Shi, L., Zhu, L., Aguirre, T., Qi, J., Chen, Y., Liu, Y., Chin, A. C., Zhu, H., Fiedler, D., et al. (2025) · Diabetes · doi:10.2337/db24-0706 · Cited by 2
AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1
Wang, H., Zhang, Q., Sun, Y., Tan, W., & Zhang, M. (2024) · Journal of Biomedical Research · doi:10.7555/jbr.38.20240244 · Cited by 1
Ghirardo, M., Cattapan, I., Sabatino, J., Pozza, A., Fumanelli, J., Avesani, M., Doblas, J. G. D. R., Moretti, C., Castaldi, B., & Salvo, G. D. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2024.1476456 · Cited by 1
Yan, F., & Bao, L. (2025) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-025-10606-1 · Cited by 1
Ma, X., Jiang, B., Wan, S.-F., & Wei, Z.-H. (2025) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2025.120676 · Cited by 2
Research progress on cellular behavior of CaSR in cardiovascular diseases
liu, X., Xie, T., Qadir, J., Li, S., Xu, T., Lu, Y., Ge, X., & Yuan, H. S. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1672536 · Cited by 1
Azarboo, A., Jalali, S., Shaker, F., Khalaji, A., Assempoor, R., Javidan, A., Mohammadi, Y., Bahrami, O., Farahmandniya, N., & Cannavò, A. (2025) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-025-02047-2 · Cited by 1
SLC31A1 exon 1 methylation reduces intracellular copper ion and promotes diabetic cardiac fibrosis
Song, K., Geng, H.-R., Liu, Z., Lin, L.-C., Tu, B., Sun, H., Mao, S., Liu, P., Sun, X., Shi, Y., et al. (2026) · Cardiovascular Diabetology · doi:10.1186/s12933-026-03124-0 · Cited by 1
The role of mitochondria-associated membranes in tumorigenesis
Zhu, Y., Tang, G., Tang, M., Zhou, B., Xu, J., Ma, X., Li, Z., Liu, G., & Han, Y. (2026) · Discover Oncology · doi:10.1007/s12672-026-04762-2 · Cited by 1
Xu, J., Hao, Y., Cao, J., Yang, X., Gao, Y., Sun, X., Nie, R., Zhong, Q., Zhong, Y., Zhong, J., et al. (2026) · EMBO Molecular Medicine · doi:10.1038/s44321-026-00422-8 · Cited by 1
Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application
Hang, N., Zhao, R., Zhang, F., Guo, D., Li, Q., Shen, Z., Gao, R., Gao, C., Xie, Z., Fu, S., et al. (2026) · MedComm · doi:10.1002/mco2.70749 · Cited by 1
Lu, L., Wang, Y., Liu, R., Fang, B., Zhao, M., Feng, F., & Wang, J. (2026) · Food Bioscience · doi:10.1016/j.fbio.2026.109148 · Cited by 1
Syntabulin promotes heart failure by enhancing SR–mitochondria tethering and impairing mitofission
Li, Y., Sun, Z., Duan, H., Wu, M., Yi, J., Wang, G., Liu, W., Zhang, C., Cheng, W., Li, J. W., et al. (2026) · Cardiovascular Research · doi:10.1093/cvr/cvag139 · Cited by 1
Flores, J., Garcia, M. V. F., Abedejos, P., Hernandez, J. A., Kha, P. T., Kim, H. K., Marquez, J. C., & Han, J. (2026) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00230.2026 · Cited by 1
AMP-activated protein kinase activation: therapeutic potential in human diseases
Xu, W., Zhang, Y., & Xiao, H. (2019) · 中国科学通报：英文版 · doi:10.1016/j.scib.2019.07.032 · Cited by 1
Endoplasmic reticulum-mitochondrial interaction and calcium homeostasis
ChuanRen, Q. U., & Lei, L. I. U. (2024) · Scientia Sinica Vitae · doi:10.1360/ssv-2024-0103 · Cited by 1
Redefining the role of autophagy in diabetic vascular diseases
An, Y., & Ren, J. T. (2024) · Exploration of Medicine · doi:10.37349/emed.2024.00249 · Cited by 1
Guedouari, H., Dia, M., Geoffray, J., Brun, C., Moulin, F., Givre, L., Belmudes, L., Léon, C., Chanon, S., Ji-Cao, J., et al. (2025) · Journal of Molecular and Cellular Cardiology Plus · doi:10.1016/j.jmccpl.2025.100453 · Cited by 2
Analysis of MTORC2 in regulating aging, metabolism and cardiac disease in Drosophila melanogaster
Chang, K. (2020) · Iowa State University Digital Repository (Iowa State University) · doi:10.31274/etd-20210114-24 · Cited by 1
Rethineswaran, V. K., Jang, W. B., Choi, J., Lim, H. J., Park, S., Lee, E. J., Ha, J. S., Yun, J., & Kwon, S. (2023) · Research Square · doi:10.21203/rs.3.rs-2903880/v1 · Cited by 1
Hou, Y., Sun, X., Gheinani, P. T., Guan, X., Sharma, S., Zhou, Y., Jin, C., Yang, Z., Naren, A. P., Yin, J., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.11.16.385765
Federico, M. (2021) · El Servicio de Difusión de la Creación Intelectual (National University of La Plata) · doi:10.35537/10915/115958
Fu, F., Chang, P., Zhang, X., Zhang, J., Wang, J., Wang, X., Li, M., Wang, R., & Yu, J. (2022) · Research Square · doi:10.21203/rs.3.rs-1976524/v1
Does endoplasmic reticulum stress break the heart?
Duttaroy, A. K., & Mallick, R. (2024) · Elsevier eBooks · doi:10.1016/b978-0-323-99570-2.00009-6
Molecular cardiopharmacology and Therapeutics-I
Tiwary, P., Oswal, K., & Kumar, D. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-16013-4.00022-1
Advances in the Study of the Role of Mitophagy in Diabetes Mellitus and Its Complications
沙, 晓. (2025) · Pharmacy Information · doi:10.12677/pi.2025.143018
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565585
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565573
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565582
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26709494
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565576
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26709482
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565564
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565570
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25658675
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565588
Chang, Y., Wang, C., Zhu, J., Zheng, S., Sun, S., Wu, Y., Jiang, X., Li, L., Ma, R., & Li, G. (2024) · Figshare · doi:10.6084/m9.figshare.26605984
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26709488
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25658648
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565558
Zhou, Q., Yang, J., Wang, W., Shao, C., Hua, X., & Tang, Y.-D. (2023) · Figshare · doi:10.6084/m9.figshare.23788373
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26709479
Chang, Y., Wang, C., Zhu, J., Zheng, S., Sun, S., Wu, Y., Jiang, X., Li, L., Ma, R., & Li, G. (2024) · Figshare · doi:10.6084/m9.figshare.26605987
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565555
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26709485
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565561
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565579
Peng, C., Zhang, Y., Lang, X., & Zhang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26565567
Ji, L., Zhang, X., Chen, Z., Wang, Y., Zhu, H., Nai, Y., Huang, Y., Lai, R., Zhong, Y., Yang, X., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26709491
Jin, Z., Ji, Y., Su, W., Zhou, L., Gao, L., Wen, X., Tang, H.-P., Xia, Z.-Y., & Lei, S. (2026) · Biochemical Pharmacology · doi:10.1016/j.bcp.2026.117835
Chen, X., Zhang, L.-L., Zhou, Y., Dong, D.-X., & Qian, X.-Y. (2026) · World Journal of Diabetes · doi:10.4239/wjd.v17.i3.112177
From Defence to Dysfunction: The Dual Role of Autophagy and Mitophagy in Cardiomyopathy
Dubey, N., Chaturvedi, G., Panchbhai, P., Singh, S., Goyal, A., Singh, N., Vishwakarma, V. K., Parakh, N., Ramakrishnan, L., & Yadav, H. N. (2026) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.70830
Xu, J., Yang, X., Cao, J., Hao, Y., Nie, R., Zhong, Q., Gao, Y., Hui, Y., Kuang, L., Zhong, Y., et al. (2026) · Science Signaling · doi:10.1126/scisignal.adx4313
GLP-1 receptor and Mitochondria-ER Contact Sites: an emerging mechanism of metabolic regulation
Cruz, P., Puebla-Huerta, A., Troncoso, M. F., Silva-Pavez, E., Hidalgo, Y., & Ahumada-Castro, U. (2026) · Frontiers in Physiology · doi:10.3389/fphys.2026.1826699
Xu, R., Ding, Z., Zhou, J., Wang, S., Yuan, J., Wu, J., Xu, Y., Wang, Q., Sun, H., & Zou, Y. (2026) · Research Square · doi:10.21203/rs.3.rs-10079014/v1
Jiang, H., Zhao, Y., Zhao, Y., Wang, S., Zhai, W., & Liu, Z. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1847325
Kang, Y., Hu, Y., Sun, X.-T., Fan, X., Li, A.-L., Shang, W.-Y., Jia, Y., Zhao, Y.-X., Miao-miao, W., Wang, T., et al. (2026) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-026-10776-6
Hou, C., Zhao, Y., Ma, Y. Q., Zhou, X., Yao, L., Li, J., Gui, M., Wang, M., Chen, X., Fu, D., et al. (2026) · Scientific Reports · doi:10.1038/s41598-026-56197-y
Rethineswaran, V. K., Hong, Y. J., Jang, W. B., Choi, J., Lim, H. J., Park, S., Lee, E. S., Ha, J. S., Yun, J., & Kwon, S. (2026) · Oxidative Medicine and Cellular Longevity · doi:10.1155/omcl/6619225
Cui, J., Wei, L., Xu, B., Han, S., Guo, C., & Wang, X. (2026) · Discover Oncology · doi:10.1007/s12672-026-05287-4
Xu, J., Cao, J., Yang, X., Hao, Y., Gao, Y., Sun, X., Nie, R., Zhong, Q., Zhong, Y., Leng, S., et al. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117550
Metadata
- Authors
- Wu, S., Lu, Q., Ding, Y., Wu, Y., Qiu, Y., Wang, P., Mao, X., Huang, K., Xie, Z., & Zou, M.-H.
- Affiliations
- Georgia State University (US)
- University of Washington (US)
- Wuhan Union Hospital (CN)
- Corresponding author
- Xie, Zhonglin
- Zou, Ming-Hui
- Venue
- Circulation
- Published
- 2019-04-16
- Volume
- 139
- Issue
- 16
- Pages
- 1913-1936
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC6465113
- OpenAlex
- W2911037090
- Semantic Scholar
- 6ae43efb25ca95c487961d8441dedd8e60e67291
- Cited by
- 298
- References
- 78
- Citations by year
- 2026: 37 · 2025: 48 · 2024: 55 · 2023: 43 · 2022: 47 · 2021: 27 · 2020: 32 · 2019: 8
- FWCI
- 9.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association (16POST31160009, 16GRANT29590003, 16POST29960011)
- University of Washington
- Georgia Research Alliance
- National Institute on Aging (AG047776, R01AG047776)
- National Heart, Lung, and Blood Institute (HL128014, HL137371, R01HL105157, HL 079584, R01HL079584, HL110488, HL140954, HL-080499, R01HL142287, R01HL137371, R01HL132500, R01HL074399, R01HL080499, HL132500, HL-089920, R01HL140954, R01HL110488, HL142287, R01HL128014, R01HL089920, CA213022, R01HL096032)
- National Cancer Institute (CA-213022, R01CA213022)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- diabetic cardiomyopathy, hyperglycemia, FUNDC1, mitochondria-associated endoplasmic reticulum membranes, IP3R2, mitochondrial calcium flux, mitophagy, AMPK, mitochondrial dysfunction, cardiomyocytes, streptozotocin-induced diabetes, Akita mice, cardiomyocyte-specific knockout, apoptosis, mitochondrial fragmentation, ubiquitination
- MeSH terms
- Adult, Aged, Animals, Cell Line, Endoplasmic Reticulum, Female, Gene Expression Regulation, Humans, Male, Membrane Proteins, Mice, Inbred C57BL, Middle Aged, Mitochondria, Myocardial Contraction, Mice, Knockout, Calcium Signaling, Mitochondrial Proteins, Myocytes, Cardiac, Mitochondrial Membranes, Mice, Rats, AMP-Activated Protein Kinases, Diabetic Cardiomyopathies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
