Modulating Human Physiology: Mitochondrial Homeostasis
Understanding the underlying mechanisms of autoimmune diseases has evolved beyond the simple reduction of surface-level inflammation. The latest trends in biomedicine indicate that mitochondria play a central role in the onset and maintenance of psoriasis. Chronic mitochondrial oxidative stress and the accumulation of degraded mitochondria lead to the release of mitochondrial DNA (mtDNA) into the cytosol, compelling keratinocytes to secrete massive cascades of inflammatory cytokines.
💡 The Concept of Asymmetric Selectivity (JAK1/TYK2)
Traditionally, the blocking of overactive immune signals is achieved through chemical inhibitors of the JAK-STAT pathway. However, a new wave of scientific research brings a cutting-edge approach to the forefront: asymmetric inhibition.
Certain key cytokines involved in psoriasis (such as IL-23 and Type I interferons) transmit their destructive signals via a specific heterodimeric complex composed of JAK1 and TYK2 receptors. Asymmetric selectivity refers to the ability to specifically block only this disease-driving complex, while sparing the JAK2/JAK2 homodimeric complex—which is crucial for the body’s normal hematopoietic (blood-forming) functions.
🎯 The Objective of the Deniplant Research Program
Building upon decades of remarkable results in managing the manifestations of psoriasis, this new scientific program aims to experimentally demonstrate how natural nanoparticles and complex phyto-carriers found in Deniplant extracts can act as natural allosteric modulators, capable of restoring cellular bioenergetic function.
📊 Pillars of the Scientific Strategy
1. Computational (In Silico) Modeling
The use of advanced bioinformatic techniques (Virtual Screening and Molecular Docking) to map the three-dimensional interaction between plant secondary metabolites (flavonoids, triterpenes, phenolic acids) and the allosteric pockets of TYK2/JAK1 (PDB IDs: 6U8D, 6P8E).
2. Biological Validation (In Vitro)
Experimental evaluation using human keratinocyte cell cultures (HaCaT) subjected to inflammatory stimulation, with direct monitoring of mitochondrial oxidative stress levels (MitoSOX Red), mitochondrial membrane integrity (JC-1), and the inhibition of STAT protein phosphorylation.
📈 Impact on Cellular Homeostasis
By combining botanical nanomedicine with cell biology, the objective is to confirm a dual mechanism of action:
- Reduction of metabolic stress: Blocking aberrant signaling via the JAK1/TYK2 axis reduces proton “leakage” and normalizes the synthesis of functional ATP.
- Activation of mitophagy: Efficient elimination of aged or dysfunctional cellular organelles to halt the autoimmune signal at its source.
Are you a research partner or from the academic community?
We provide preliminary in vitro testing protocols and computational maps to partner laboratories and universities interested in expanding research into botanical nanomedicine.
Contact the Center for Biomedicine