كيناز المرتبط بمستقبل إنترلوكين-1 2 هو منظم وظيفي لأسفل لعامل التكميل د الذي يتحكم في صحة الميتوكوندريا في اعتلال عضلة القلب السكري

  • role: First author第一作者
  • Affiliation:

    Department of Medicine, Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA

Stanislovas S. Jankauskas1,  
  • Affiliation:

    Department of Molecular Pharmacology, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, New York, NY 10461, USA

Fahimeh Varzideh2,  
  • Affiliation:

    Department of Molecular Pharmacology, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, New York, NY 10461, USA

Pasquale Mone2,  
  • Affiliation:

    Department of Medicine, Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA

Urna Kansakar1,  
  • Affiliation:

    Department of Medicine, Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA

Francesco Di Lorenzo1,  
  • Affiliation:

    Department of Medicine, Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA

Angela Lombardi1,  
  • role: Corresponding author通信作者
  • Affiliation:

    Department of Medicine, Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Einstein Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA

    Department of Molecular Pharmacology, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, New York, NY 10461, USA

  • Email:gsantulli001@gmail.com
  • Introduction:*gsantulli001@gmail.com
Gaetano Santulli12*

ملخص

مفهوم

Adipsin;Complement factor D;interleukin-1;Interleukin-1 receptor-associated kinase like 2 (Irak2);Opa1;Prohibitin (PHB)

References

  1. 1..
    Jankauskas SS, Kansakar U, Varzideh F, Wilson S, Mone P, Lombardi A, et al. Heart failure in diabetes. Metabolism. 2021;125:154910.
  2. 2..
    Jiang MY, Man WR, Zhang XB, Zhang XH, Duan Y, Lin J, et al. Adipsin inhibits Irak2 mitochondrial translocation and improves fatty acid β-oxidation to alleviate diabetic cardiomyopathy. Mil Med Res. 2023;10(1):63.
  3. 3..
    Barthelemy J, Bogard G, Wolowczuk I. Beyond energy balance regulation: the underestimated role of adipose tissues in host defense against pathogens. Front Immunol. 2023;14:1083191.
  4. 4..
    Alex L, Tuleta I, Hanna A, Frangogiannis NG. Diabetes induces cardiac fibroblast activation, promoting a matrix-preserving nonmyofibroblast phenotype, without stimulating pericyte to fibroblast conversion. J Am Heart Assoc. 2023;12(6):e027463.
  5. 5..
    de Rosa M, Gambardella J, Shu J, Santulli G. Dietary fat is a key determinant in balancing mitochondrial dynamics in heart failure: a novel mechanism underlying the obesity paradox. Cardiovasc Res. 2018;114(7):925–7.
  6. 6..
    Milek M, Moulla Y, Kern M, Stroh C, Dietrich A, Schon MR, et al. Adipsin serum concentrations and adipose tissue expression in people with obesity and type 2 diabetes. Int J Mol Sci. 2022;23(4):2222.
  7. 7..
    Zhou H, Wang H, Yu M, Schugar RC, Qian W, Tang F, et al. IL-1 induces mitochondrial translocation of IRAK2 to suppress oxidative metabolism in adipocytes. Nat Immunol. 2020;21(10):1219–31.
  8. 8..
    Freeman HC, Hugill A, Dear NT, Ashcroft FM, Cox RD. Deletion of nicotinamide nucleotide transhydrogenase: a new quantitive trait locus accounting for glucose intolerance in C57BL/6J mice. Diabetes. 2006;55(7):2153–6.
  9. 9..
    Williams JL, Hall CL, Meimaridou E, Metherell LA. Loss of Nnt increases expression of oxidative phosphorylation complexes in C57BL/6J hearts. Int J Mol Sci. 2021;22(11):6101.
  10. 10..
    Close AF, Chae H, Jonas JC. The lack of functional nicotinamide nucleotide transhydrogenase only moderately contributes to the impairment of glucose tolerance and glucose-stimulated insulin secretion in C57BL/6J vs. C57BL/6N mice. Diabetologia. 2021;64(11):2550–61.

قراءة النص الكامل

The above content is generated by Large Model Translation. The translated content is for reference only. We do not assume any commercial or legal responsibilty for any consequences arising from the use of our website