In modern aesthetic medicine, true innovation is no longer measured solely by the ability to fill or tighten the skin, but by its potential to reactivate the biological mechanisms of cellular regeneration. At the core of this process are the mitochondria—the “powerhouses” of our cells—whose function is essential to maintaining skin vitality and health.
The role of mitochondria in the skin
Through cellular respiration, mitochondria convert oxygen and glucose into Adenosine Triphosphate (ATP), the energy currency that enables cells to repair, regenerate, and maintain balance.
But their role goes far beyond energy production, as they perform crucial signaling functions within the body:
- Regulate cellular calcium levels.
- Control apoptosis (programmed cell death).
- Act as primary regulators of oxygen homeostasis.
- Are involved in processes such as growth, aging, and adaptive responses.
The root of aging: mitochondrial slowdown and “Inflammaging”
When this energy machinery begins to fail, cellular metabolism slows, triggering a state of low-grade chronic inflammation known as inflammaging. This process is characterized by persistent microinflammation that accelerates dermal tissue degradation and promotes the appearance of wrinkles, spots, and sagging.
Mitochondrial dysfunction, especially when caused by a lack of oxygen (hypoxia or ischemia), disrupts cellular homeostasis and unleashes a cascade of metabolic anomalies. This imbalance increases the risk of chronic diseases, encourages neurodegeneration and insulin resistance, and can ultimately lead to necrosis or cell death.
At this point, a key metabolite emerges—one that bridges metabolism, signaling, and cellular response: succinic acid.
Succinic acid: a metabolic modulator and driver of cellular bioenergy
Succinic acid is a critical intermediate in the Krebs cycle (or tricarboxylic acid cycle, TCA), a process that occurs in the mitochondrial matrix and lies at the heart of cellular respiration. Beyond its role in energy production, this metabolite acts as a metabolic modulator capable of reactivating mitochondrial function, stimulating autophagy and mitophagy, and enhancing communication between fibroblasts and adipocytes.
These actions promote the synthesis of type III collagen and growth factors, helping cells recover their youthful behavior and maintain their energetic and regenerative capabilities.
Inbiotec Amber: regenerative science applied to cellular energy
From this perspective emerges Inbiotec Amber, IT Pharma’s first “skin builder.” The key to rejuvenation lies in “rehabilitating” the dermal ecosystem. Its formula combines two 100% biocompatible and naturally occurring actives in the body: hyaluronic acid (HA) and succinic acid.
- Hyaluronic acid, high molecular weight non-crosslinked (≈ 2 MDa, 1.1%) with hydrating, soothing, and antioxidant effects.
- Succinic acid (1.6%), a key metabolite of the Krebs cycle, responsible for activating mitochondrial function and stimulating cellular regeneration. The true star of this product.
Evidence and results
In vitro studies have demonstrated that the HA + succinic acid combination acts synergistically:
- Mitochondrial reactivation: Stimulates mitochondrial function by boosting the Krebs cycle. The Krebs cycle is fundamental to cellular respiration, converting pyruvate into ATP and other energy molecules.
- Fibroblast regeneration: This metabolic stimulation aims to reverse the metabolic slowdown and increase the number and activity of fibroblasts—cells critical for collagen and elastin production.
- Combats Inflammaging: Succinic acid provides a powerful anti-inflammatory and antioxidant effect. It helps reduce the release of inflammatory cytokines in damaged skin and neutralizes free radicals.
- Depigmenting effect: Succinic acid has a remarkable ability to reduce hyperpigmentation by chelating copper ions in the tyrosinase enzyme of melanocytes, thus blocking melanin production.
Together, this synergy “reprograms” aged cells, inducing renewal processes and encouraging cells to behave more youthfully—addressing aging at its root.
Bibliographic references
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Huang, H., Li, G., He, Y., Chen, J., Yan, J., Zhang, Q., Li, L., & Cai, X. (2024). Cellular succinate metabolism and signaling in inflammation: Implications for therapeutic intervention. Frontiers in Immunology, 15, 1404441. https://doi.org/10.3389/fimmu.2024.1404441
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Trauelsen, M., Hiron, T. K., Lin, D., Petersen, J. E., Breton, B., Husted, A. S., et al. (2021). Extracellular succinate hyperpolarizes M2 macrophages through SUCNR1/GPR91-mediated Gq signaling. Cell Reports, 35(10), 109246. https://doi.org/10.1016/j.celrep.2021.109246
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de Castro Fonseca, M., Aguiar, C. J., da Rocha Franco, J. A., Gingold, R. N., & Leite, M. F. (2016). GPR91: Expanding the frontiers of Krebs cycle intermediates. Cell Communication and Signaling, 14, 3. https://doi.org/10.1186/s12964-016-0126-1
Papurina, T., Barsukov, O., Zabuga, O., Krasnienkov, D., & Denis, E. (2023). Effects of succinic acid on dermal fibroblasts during cultivation under extremely hypoxic conditions. Biochemistry and Biophysics Reports, 33, 101429. https://doi.org/10.1016/j.bbrep.2023.101429
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