Citrate-Ascorbate Synthesis

Ascorbate (C6H8O6)
Citrate (C6H8O7)

Ascorbate
Ascorbic Acid

Dihydroxyethyl
Dihydroxyfuran

Furan
Lactone
Ketogluconic Acid
Enediol
Carbonyl

Ascorbic acid is a furan-based lactone of 2-ketogluconic acid. It contains an adjacent enediol adjacent to the carbonyl.

Ascorbate Peroxidase
Ascorbate Ferrireductase
Ascorbate Dioxygenase
Ascorbate Oxidase
Glutathione-Ascorbate Cycle

Transmembrane

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https://en.m.wikipedia.org/wiki/Chemistry_of_ascorbic_acid

https://en.m.wikipedia.org/wiki/Mineral_ascorbates

https://en.m.wikipedia.org/wiki/Ascorbate_peroxidase

https://en.m.wikipedia.org/wiki/Ascorbate_ferrireductase_(transmembrane)

https://en.m.wikipedia.org/wiki/Ascorbate_2,3-dioxygenase

https://en.m.wikipedia.org/wiki/L-ascorbate_oxidase

https://en.m.wikipedia.org/wiki/Glutathione-ascorbate_cycle

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Potassium Citrate
Magnesium Sulfate

Recent Updates on Anti-Inflammatory and Antimicrobial Effects of Furan Natural Derivatives

https://pmc.ncbi.nlm.nih.gov/articles/PMC7443407/

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Vagus Nerve
DMSO

Collagen
Elastin
Proteoglycans
Glucosamine
Chondroitin

https://www.americancancercenternigeria.com/shop/item.aspx?itemid=2

The vagus nerve and the inflammatory reflex—linking immunity and metabolism

https://pmc.ncbi.nlm.nih.gov/articles/PMC4082307/

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Calcium (Ca2+)
Hypercalcemia
Intracellular
Signaling Molecules
Calcification
Mitochondria
Cellular Senescence

Regulation and role of calcium in cellular senescence

https://www.sciencedirect.com/science/article/abs/pii/S0143416023000131

Mitochondrial Dysfunction: Cause or Consequence of Vascular Calcification

https://pmc.ncbi.nlm.nih.gov/articles/PMC8010668/

Microglial Potassium Channels: From Homeostasis to Neurodegeneration

https://pmc.ncbi.nlm.nih.gov/articles/PMC8698630/

Neuroinflammation: The Devil is in the Details

https://pmc.ncbi.nlm.nih.gov/articles/PMC5025335/

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Lipedema
Edema
Glycogen
Phosphocreatine
Bioenergetic Systems

https://www.lipedema.org/research-grants/

https://morethanfat.com/lipedema-and-nutrition/lipedema-nutrition-and-common-supplements

Renal Dysfunction in Cirrhosis: Diagnosis, Treatment, and Prevention

https://pmc.ncbi.nlm.nih.gov/articles/PMC1480573/

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Cold Shock Proteins
Y-Box Binding Protein
YB-1
DNA Binding Protein B
DbpB
M4 ipRGCs
Potassium
DMSO
Methylene Blue
Blue Light
Optogenetics
Melanopsin
Leptin
Cytokine
Endocrine System
Vagus Nerve

Cold shock proteins: from cellular mechanisms to pathophysiology and disease

https://biosignaling.biomedcentral.com/articles/10.1186/s12964-018-0274-6

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Potassium
Hyperpolarization
GABA-B Receptor
G Protein
Guanine Nucleotide
Binding Protein
Coupled Receptor
GTPase
Intracellular

Potassium channel-based optogenetic silencing

https://pmc.ncbi.nlm.nih.gov/articles/PMC6218482/

Optogenetics. Engineering of a light-gated potassium channel

blue-light-induced K(+) channel 1 (BLINK1) engineered by fusing the plant LOV2-Jα photosensory module to the small viral K(+) channel Kcv. BLINK1 exhibits biophysical features of Kcv, including K(+) selectivity and high single-channel conductance but reversibly photoactivates in blue light. Opening of BLINK1 channels hyperpolarizes the cell to the K(+) equilibrium potential.

https://en.m.wikipedia.org/wiki/Hyperpolarization_(biology)

https://en.m.wikipedia.org/wiki/GABAB_receptor

https://en.m.wikipedia.org/wiki/G_protein-coupled_receptor

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Mitochondrial osmoregulation in evolution, cation transport and metabolism

https://www.sciencedirect.com/science/article/pii/S0005272821000013

As organisms evolved to have less sodium cations abundant cytosols and replace Na+ with K+ and over time with other osmolytic solutes, mitochondria were forced to keep pace in eukaryotes. Thus, mitochondria became more dependent on potassium cations as the major osmolyte.

The nitrogen–potassium intersection: membranes, metabolism, and mechanism

https://onlinelibrary.wiley.com/doi/10.1111/pce.12671

Nitrogen is an essential constituent of a vast array of metabolites and structural compounds, including proteins, nucleic acids, chlorophyll, co-enzymes, phytohormones and secondary metabolites, while the main functions of K+ are as a major osmolyte and source of positive charge for electrical homeostasis and enzyme activation.

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WHAT ARE THE CONCENTRATIONS OF DIFFERENT IONS IN CELLS?

https://book.bionumbers.org/what-are-the-concentrations-of-different-ions-in-cells/

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Toxic
DNA Adduction
Mallard Reaction
Thiamine
Nucleotide
Asparagine
Acrylamide
Glycidamide
Oxiranecarboxamide
Amyloid
Synuclein
Lipofuscin

Heparan Sulfate
Glucosaminide
Glycosaminoglycan

Glycidamide inhibits the sodium/potassium ATPase protein present in the plasma membrane of nerve cells. Intracellular sodium increases and intracellular potassium decreases due to this inhibition. This causes depolarization of the nerve membrane. The depolarization triggers a reverse sodium/calcium exchange, which will cause calcium-mediated axon degeneration.

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N-acetylcysteine for chronic kidney disease: a systematic review and meta-analysis

https://pmc.ncbi.nlm.nih.gov/articles/PMC8129408/

The role of leptin in selected skin diseases

https://pmc.ncbi.nlm.nih.gov/articles/PMC7532589/

Molecule interacts with prion proteins to alter cell behaviour

https://www.ualberta.ca/en/medicine/news/2014/april/prion-proteins-potassium-channels.html

Lipofuscin-bound iron is a major intracellular source of oxidants: Role in senescent cells

https://www.sciencedirect.com/science/article/abs/pii/S0891584910000638

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Intracellular
Extracellular

Lipofuscin
Glycidamide

vs

Amyloidosis
Prion

Role of Intracellular Amyloid β as Pathway Modulator, Biomarker, and Therapy Target

https://pmc.ncbi.nlm.nih.gov/articles/PMC9103247/

Research in recent decades focused on the pathological role of extracellular amyloid β aggregation, widely neglecting the potential meaning of very early generation of amyloid β inside the cell.

A central hallmark of the disease is the presence of amyloidogenic plaques, formed by deposition, accumulation, and aggregation of the amyloid β peptide (Aβ) in the brain. The second well-described pathophysiological characteristic are neurofibrillary tangles, which result from hyperphosphorylation of the microtubule-associated Tau protein, consequently leading to cytoskeletal changes in neurons.