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Related Concept Videos

ATP Synthase: Mechanism01:48

ATP Synthase: Mechanism

In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased ATP...
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Mechanisms Involved in Pathological Succinate-Mediated Signaling.

Bismarck Bernabe-Yepes1, Cecilia Zazueta1

  • 1Departamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No. 1 Tlalpan, Mexico City 14080, Mexico.

International Journal of Molecular Sciences
|May 27, 2026
PubMed
Summary

Extracellular succinate acts as a signaling molecule via succinate receptor 1 (SUCNR1). Its signaling pathways show context-dependent effects, influencing inflammation and metabolic regulation in various diseases.

Keywords:
DAMPSUCNR1biomarkerinflammationsuccinate

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Area of Science:

  • Biochemistry
  • Cellular Biology
  • Metabolic Regulation

Background:

  • Succinate is a Krebs cycle intermediate with emerging roles beyond energy metabolism.
  • Extracellular succinate functions as a signaling molecule through succinate receptor 1 (SUCNR1).
  • SUCNR1 signaling exhibits significant heterogeneity across different pathological contexts.

Purpose of the Study:

  • To comprehensively analyze SUCNR1 signaling pathways activated by succinate.
  • To explore the context-dependent nature of succinate-SUCNR1 interactions.
  • To evaluate the therapeutic potential of modulating succinate signaling in diseases.

Main Methods:

  • Literature review of studies on succinate and SUCNR1.
  • Analysis of signaling pathways involved in succinate-SUCNR1 interactions.
  • Examination of biological outcomes in various pathological conditions.

Main Results:

  • Succinate-SUCNR1 signaling influences inflammation, cellular signaling, and metabolic regulation.
  • Biological outcomes of SUCNR1 activation are varied and context-dependent.
  • Heterogeneity in SUCNR1 signaling contributes to disease progression.

Conclusions:

  • Succinate's role extends beyond metabolism, impacting disease pathogenesis via SUCNR1.
  • Understanding the context-dependent nature of succinate signaling is crucial.
  • Targeting succinate-SUCNR1 pathways may offer therapeutic strategies for various diseases.