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How human cellular healing works — a concise, evidence-based overview
1) Core idea — healing is a coordinated cellular program
Tissue repair and recovery are not single events but coordinated programs that restore homeostasis across cells, mitochondria, immune cells and extracellular matrix. Successful healing requires: (a) removal of damaged material, (b) resolution of inflammation, (c) mitochondrial and metabolic recovery, and (d) regeneration or remodelling of parenchymal and stromal cells.  

2) Damage removal: autophagy and mitophagy clear the damaged parts
Autophagy (bulk and selective) and mitophagy (selective mitochondrial autophagy) remove misfolded proteins, damaged organelles and dysfunctional mitochondria. This clearance prevents ongoing reactive oxygen species (ROS) production and stops maladaptive chronic inflammation; it also provides metabolic substrates for reparative processes. Sirtuin family proteins (SIRT1–SIRT3 etc.) are important regulators of autophagy/mitophagy and link nutrient/redox sensing to the clearance machinery.  

3) Energy recovery: mitochondria, biogenesis and quality control
Mitochondrial function underpins cellular repair. When mitochondria are damaged, ATP production falls and ROS rises, which impairs cell signalling and tissue function. Cells respond by: (a) activating mitophagy to remove defective mitochondria, (b) increasing mitochondrial biogenesis via PGC-1α pathways, and (c) shifting metabolic fluxes (AMPK/mTOR balance) to support repair rather than growth. Restored mitochondrial quality and numbers are essential for sustained tissue recovery.  

4) Inflammation → resolution: active mediators drive clean repair
Acute inflammation is required to contain damage, but exit from inflammation (resolution) is an active biochemical process driven by specialized pro-resolving mediators (SPMs: resolvins, protectins, maresins). SPMs promote efferocytosis (clearance of apoptotic cells), limit collateral tissue damage, and stimulate regenerative programs — their temporal production is central to a transition from inflammatory to reparative states. Failure to generate resolution signals contributes to chronic wounds and fibrosis.  

5) Metabolic regulators set the pace: NAD⁺, sirtuins, AMPK and mTOR
NAD⁺ levels and sirtuin activity act as metabolic rheostats. High NAD⁺/sirtuin signalling promotes DNA repair, deacetylation of autophagy proteins, and mitochondrial quality control. AMPK activation signals low-energy states and promotes autophagy/mitochondrial biogenesis, while mTOR activity promotes growth and suppresses autophagy. The dynamic interplay between these sensors determines whether a cell invests resources in clean-up and repair (autophagy/biogenesis) or in proliferation and extracellular matrix deposition.  

6) Cellular plasticity and regeneration: progenitors, stem niches and local signals
Regeneration depends on local progenitor and stem cells (e.g., satellite cells in muscle, neural progenitors in certain brain regions). Their activation requires a permissive metabolic and inflammatory milieu: cleared debris, resolved inflammation, sufficient mitochondrial function and pro-regenerative growth factors. Excessive or prolonged inflammatory signalling biases tissue toward scarring/fibrosis rather than functional regeneration.  

7) Systems interplay — why multi-target approaches work
Because healing engages immune, metabolic, autophagic and progenitor systems simultaneously, interventions that act on multiple nodes (e.g., reduce oxidative stress, promote mitophagy, modulate HPA/ cortisol signaling, and enhance pro-resolution mediators) are more likely to restore functional homeostasis than single-target approaches. This is the rationale behind integrative strategies that combine lifestyle, metabolic cofactors and targeted botanicals or extracts in measured doses.    

How human cellular healing works — a concise, evidence-based overview
1) Core idea — healing is a coordinated cellular program
Tissue repair and recovery are not single events but coordinated programs that restore homeostasis across cells, mitochondria, immune cells and extracellular matrix. Successful healing requires: (a) removal of damaged material, (b) resolution of inflammation, (c) mitochondrial and metabolic recovery, and (d) regeneration or remodelling of parenchymal and stromal cells.  

2) Damage removal: autophagy and mitophagy clear the damaged parts
Autophagy (bulk and selective) and mitophagy (selective mitochondrial autophagy) remove misfolded proteins, damaged organelles and dysfunctional mitochondria. This clearance prevents ongoing reactive oxygen species (ROS) production and stops maladaptive chronic inflammation; it also provides metabolic substrates for reparative processes. Sirtuin family proteins (SIRT1–SIRT3 etc.) are important regulators of autophagy/mitophagy and link nutrient/redox sensing to the clearance machinery.  

3) Energy recovery: mitochondria, biogenesis and quality control
Mitochondrial function underpins cellular repair. When mitochondria are damaged, ATP production falls and ROS rises, which impairs cell signalling and tissue function. Cells respond by: (a) activating mitophagy to remove defective mitochondria, (b) increasing mitochondrial biogenesis via PGC-1α pathways, and (c) shifting metabolic fluxes (AMPK/mTOR balance) to support repair rather than growth. Restored mitochondrial quality and numbers are essential for sustained tissue recovery.  

4) Inflammation → resolution: active mediators drive clean repair
Acute inflammation is required to contain damage, but exit from inflammation (resolution) is an active biochemical process driven by specialized pro-resolving mediators (SPMs: resolvins, protectins, maresins). SPMs promote efferocytosis (clearance of apoptotic cells), limit collateral tissue damage, and stimulate regenerative programs — their temporal production is central to a transition from inflammatory to reparative states. Failure to generate resolution signals contributes to chronic wounds and fibrosis.  

5) Metabolic regulators set the pace: NAD⁺, sirtuins, AMPK and mTOR
NAD⁺ levels and sirtuin activity act as metabolic rheostats. High NAD⁺/sirtuin signalling promotes DNA repair, deacetylation of autophagy proteins, and mitochondrial quality control. AMPK activation signals low-energy states and promotes autophagy/mitochondrial biogenesis, while mTOR activity promotes growth and suppresses autophagy. The dynamic interplay between these sensors determines whether a cell invests resources in clean-up and repair (autophagy/biogenesis) or in proliferation and extracellular matrix deposition.  

6) Cellular plasticity and regeneration: progenitors, stem niches and local signals
Regeneration depends on local progenitor and stem cells (e.g., satellite cells in muscle, neural progenitors in certain brain regions). Their activation requires a permissive metabolic and inflammatory milieu: cleared debris, resolved inflammation, sufficient mitochondrial function and pro-regenerative growth factors. Excessive or prolonged inflammatory signalling biases tissue toward scarring/fibrosis rather than functional regeneration.  

7) Systems interplay — why multi-target approaches work
Because healing engages immune, metabolic, autophagic and progenitor systems simultaneously, interventions that act on multiple nodes (e.g., reduce oxidative stress, promote mitophagy, modulate HPA/ cortisol signaling, and enhance pro-resolution mediators) are more likely to restore functional homeostasis than single-target approaches. This is the rationale behind integrative strategies that combine lifestyle, metabolic cofactors and targeted botanicals or extracts in measured doses.    

How human cellular healing works — a concise, evidence-based overview
1) Core idea — healing is a coordinated cellular program
Tissue repair and recovery are not single events but coordinated programs that restore homeostasis across cells, mitochondria, immune cells and extracellular matrix. Successful healing requires: (a) removal of damaged material, (b) resolution of inflammation, (c) mitochondrial and metabolic recovery, and (d) regeneration or remodelling of parenchymal and stromal cells.  

2) Damage removal: autophagy and mitophagy clear the damaged parts
Autophagy (bulk and selective) and mitophagy (selective mitochondrial autophagy) remove misfolded proteins, damaged organelles and dysfunctional mitochondria. This clearance prevents ongoing reactive oxygen species (ROS) production and stops maladaptive chronic inflammation; it also provides metabolic substrates for reparative processes. Sirtuin family proteins (SIRT1–SIRT3 etc.) are important regulators of autophagy/mitophagy and link nutrient/redox sensing to the clearance machinery.  

3) Energy recovery: mitochondria, biogenesis and quality control
Mitochondrial function underpins cellular repair. When mitochondria are damaged, ATP production falls and ROS rises, which impairs cell signalling and tissue function. Cells respond by: (a) activating mitophagy to remove defective mitochondria, (b) increasing mitochondrial biogenesis via PGC-1α pathways, and (c) shifting metabolic fluxes (AMPK/mTOR balance) to support repair rather than growth. Restored mitochondrial quality and numbers are essential for sustained tissue recovery.  

4) Inflammation → resolution: active mediators drive clean repair
Acute inflammation is required to contain damage, but exit from inflammation (resolution) is an active biochemical process driven by specialized pro-resolving mediators (SPMs: resolvins, protectins, maresins). SPMs promote efferocytosis (clearance of apoptotic cells), limit collateral tissue damage, and stimulate regenerative programs — their temporal production is central to a transition from inflammatory to reparative states. Failure to generate resolution signals contributes to chronic wounds and fibrosis.  

5) Metabolic regulators set the pace: NAD⁺, sirtuins, AMPK and mTOR
NAD⁺ levels and sirtuin activity act as metabolic rheostats. High NAD⁺/sirtuin signalling promotes DNA repair, deacetylation of autophagy proteins, and mitochondrial quality control. AMPK activation signals low-energy states and promotes autophagy/mitochondrial biogenesis, while mTOR activity promotes growth and suppresses autophagy. The dynamic interplay between these sensors determines whether a cell invests resources in clean-up and repair (autophagy/biogenesis) or in proliferation and extracellular matrix deposition.  

6) Cellular plasticity and regeneration: progenitors, stem niches and local signals
Regeneration depends on local progenitor and stem cells (e.g., satellite cells in muscle, neural progenitors in certain brain regions). Their activation requires a permissive metabolic and inflammatory milieu: cleared debris, resolved inflammation, sufficient mitochondrial function and pro-regenerative growth factors. Excessive or prolonged inflammatory signalling biases tissue toward scarring/fibrosis rather than functional regeneration.  

7) Systems interplay — why multi-target approaches work
Because healing engages immune, metabolic, autophagic and progenitor systems simultaneously, interventions that act on multiple nodes (e.g., reduce oxidative stress, promote mitophagy, modulate HPA/ cortisol signaling, and enhance pro-resolution mediators) are more likely to restore functional homeostasis than single-target approaches. This is the rationale behind integrative strategies that combine lifestyle, metabolic cofactors and targeted botanicals or extracts in measured doses.