Vasopressin: A Comprehensive Literature Review of Antidiuretic Hormone and Clinical Pharmacology

1. Introduction and Historical Perspective

Vasopressin, a nine-amino acid peptide hormone, has been central to our understanding of neuroendocrine physiology for over a century. First discovered in 1895 by Oliver and Schäfer, who identified its pressor effects in animal models, vasopressin was subsequently isolated from the posterior pituitary gland and characterized structurally by du Vigneaud in 1953, work that earned him the Nobel Prize in Chemistry. The hormone's dual nomenclature reflects its principal physiological actions: "vasopressin" refers to its vasoconstrictive properties, while "antidiuretic hormone" (ADH) emphasizes its crucial role in renal water conservation.

The historical trajectory of vasopressin research has been marked by several paradigm shifts in understanding. Early investigations focused primarily on its cardiovascular effects, but subsequent research revealed that its antidiuretic function represents the hormone's most critical physiological role under normal conditions. The identification of multiple receptor subtypes in the 1980s and 1990s revolutionized the field, explaining the diverse physiological and pharmacological effects of vasopressin and enabling the development of selective receptor agonists and antagonists with targeted therapeutic applications.

Contemporary research has expanded beyond classical endocrine functions to explore vasopressin's involvement in social behavior, stress responses, circadian rhythms, and cognitive processes. The hormone's clinical applications have similarly expanded from treating diabetes insipidus to managing septic shock, bleeding disorders, and various cardiovascular emergencies. This literature review synthesizes current knowledge regarding vasopressin's molecular mechanisms, receptor pharmacology, physiological roles, and clinical applications, while identifying promising directions for future research and therapeutic development.

2. Molecular Structure and Biosynthesis

Vasopressin is a nonapeptide with the amino acid sequence Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2, characterized by a disulfide bridge between the two cysteine residues at positions 1 and 6, creating a six-amino acid ring structure with a three-amino acid tail. This cyclic structure is essential for biological activity and receptor binding. In most mammals, including humans, the hormone exists as arginine vasopressin (AVP), with arginine at position 8, while some species produce lysine vasopressin with lysine at this position. The C-terminal glycine is amidated, a post-translational modification crucial for biological activity.

The biosynthesis of vasopressin occurs in magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus. The AVP gene, located on chromosome 20 in humans, encodes a 164-amino acid preprohormone consisting of a signal peptide, the vasopressin moiety, neurophysin II (a carrier protein), and copeptin (a glycopeptide). This precursor undergoes proteolytic processing during axonal transport to the posterior pituitary, where the mature hormone is stored in neurosecretory granules until released into the systemic circulation in response to appropriate stimuli.

The synthesis and secretion of vasopressin are regulated by multiple physiological factors. Osmoreceptors in the organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO) detect increases in plasma osmolality as small as 1-2%, triggering vasopressin release when osmolality exceeds approximately 280-290 mOsm/kg. Baroreceptors in the carotid sinus and aortic arch detect decreases in blood volume or pressure, providing another major regulatory input. Additional modulatory factors include angiotensin II, nausea, pain, stress, and various pharmacological agents. The exquisite sensitivity of this regulatory system maintains plasma osmolality within a narrow range of 280-295 mOsm/kg under normal physiological conditions.

3. Receptor Pharmacology and Signal Transduction

Vasopressin exerts its diverse physiological effects through interaction with three main receptor subtypes: V1a, V1b (also called V3), and V2 receptors, all members of the G protein-coupled receptor (GPCR) superfamily. These receptors exhibit distinct tissue distributions, signaling mechanisms, and physiological functions, providing the molecular basis for vasopressin's pleiotropic effects and enabling the development of selective pharmacological agents.

V1a receptors are widely distributed throughout the body, with particularly high expression in vascular smooth muscle, liver, platelets, and the central nervous system. Upon vasopressin binding, V1a receptors couple to Gq proteins, activating phospholipase C (PLC), which catalyzes the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) to generate inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 mobilizes intracellular calcium stores, while DAG activates protein kinase C (PKC). In vascular smooth muscle, this signaling cascade produces vasoconstriction, accounting for vasopressin's pressor effects. The affinity of V1a receptors for vasopressin is in the low nanomolar range (Kd approximately 1-2 nM), consistent with the hormone's potent physiological effects at circulating concentrations typically ranging from 1-5 pg/mL under basal conditions.

V1b receptors, predominantly expressed in the anterior pituitary gland, also couple to Gq proteins and activate the PLC-IP3-DAG pathway. These receptors mediate vasopressin's role in stimulating adrenocorticotropic hormone (ACTH) release from corticotrophs, contributing to stress responses and hypothalamic-pituitary-adrenal (HPA) axis regulation. V1b receptors are also found in the central nervous system, particularly in limbic regions, where they modulate stress-related behaviors and social recognition.

V2 receptors, expressed predominantly in the basolateral membrane of principal cells in the renal collecting duct, couple to Gs proteins and activate adenylyl cyclase, increasing intracellular cyclic AMP (cAMP) levels. The resulting activation of protein kinase A (PKA) phosphorylates aquaporin-2 (AQP2) water channels, promoting their translocation from intracellular vesicles to the apical membrane. This process dramatically increases water permeability of the collecting duct, enabling water reabsorption along the osmotic gradient established by the countercurrent multiplication system in the renal medulla. The V2 receptor-mediated antidiuretic effect represents vasopressin's most critical physiological function, with receptor mutations causing nephrogenic diabetes insipidus, a condition characterized by profound polyuria and polydipsia.

4. Physiological Functions and Homeostatic Regulation

The physiological functions of vasopressin extend across multiple organ systems, with its most essential role being the regulation of body fluid osmolality and volume. Under normal conditions, vasopressin secretion maintains plasma osmolality within the narrow range of 280-295 mOsm/kg through its antidiuretic effects on the kidney. When plasma osmolality increases, osmoreceptors trigger vasopressin release, which acts on V2 receptors in the collecting duct to increase water reabsorption, diluting body fluids back toward normal osmolality. Conversely, decreased osmolality suppresses vasopressin secretion, allowing dilute urine production and excretion of excess water.

The relationship between plasma vasopressin concentration and urine osmolality follows a sigmoidal curve, with maximal urinary concentration achieved at vasopressin levels of approximately 5 pg/mL. Beyond this threshold, further increases in vasopressin do not enhance antidiuresis, but may produce cardiovascular effects through V1a receptor activation. The system demonstrates remarkable sensitivity, with plasma vasopressin concentrations increasing exponentially in response to small increases in osmolality above the threshold of approximately 280 mOsm/kg, while remaining suppressed at lower osmolalities to permit water diuresis.

Vasopressin also participates in cardiovascular regulation, particularly during hypovolemia and hypotension. While the hormone's vasoconstrictor effects are generally minimal under normal physiological conditions due to low circulating concentrations and baroreceptor-mediated inhibition of secretion, vasopressin becomes an important pressor hormone during severe hemorrhage, septic shock, and other conditions characterized by profound hypotension. In these circumstances, vasopressin levels can increase 100-1000 fold, producing significant V1a receptor-mediated vasoconstriction that contributes to blood pressure maintenance.

Additional physiological functions include hepatic glycogenolysis and gluconeogenesis mediated by V1a receptors, platelet aggregation contributing to hemostasis, and central nervous system effects on social behavior, stress responses, and circadian rhythms. In the anterior pituitary, V1b receptor activation synergizes with corticotropin-releasing hormone (CRH) to stimulate ACTH secretion, particularly during stress. These diverse functions illustrate vasopressin's role as a multifunctional hormone integrating osmotic, hemodynamic, metabolic, and behavioral responses to maintain homeostasis.

5. Clinical Pharmacology: Diabetes Insipidus

Diabetes insipidus (DI) represents the prototypical disorder of vasopressin physiology and provides the primary indication for vasopressin replacement therapy. This condition, characterized by the excretion of large volumes of dilute urine (polyuria) and consequent excessive thirst (polydipsia), exists in two principal forms: central (neurogenic) diabetes insipidus, resulting from deficient vasopressin secretion, and nephrogenic diabetes insipidus, resulting from renal resistance to vasopressin's effects.

Central diabetes insipidus may result from various etiologies including neurosurgery (particularly transsphenoidal pituitary surgery), traumatic brain injury, infiltrative diseases (sarcoidosis, histiocytosis X), tumors affecting the hypothalamic-pituitary axis, autoimmune hypophysitis, and genetic mutations affecting the vasopressin gene or magnocellular neuron development. Patients typically present with urine output exceeding 3-4 liters per day, urine osmolality below 200 mOsm/kg despite elevated plasma osmolality, and plasma sodium concentrations that may be elevated if water intake is insufficient to match urinary losses. The water deprivation test, demonstrating failure to concentrate urine despite rising plasma osmolality, followed by a robust response to exogenous vasopressin administration, confirms the diagnosis.

Desmopressin (1-deamino-8-D-arginine vasopressin, DDAVP), a synthetic vasopressin analogue, represents the treatment of choice for central diabetes insipidus. Structural modifications including deamination of the N-terminal cysteine and substitution of D-arginine for L-arginine at position 8 confer enhanced V2 receptor selectivity (approximately 3000-fold versus V1a receptors) and markedly prolonged duration of action compared to native vasopressin. These modifications result from increased resistance to enzymatic degradation by peptidases, particularly aminopeptidases. Desmopressin can be administered via intranasal, oral, subcutaneous, or intravenous routes, with typical dosing ranging from 10-40 micrograms intranasally once or twice daily, or 0.1-0.4 mg orally two to three times daily, titrated to achieve normal urine output and plasma sodium concentration.

The primary adverse effect of desmopressin therapy is hyponatremia resulting from excessive water retention, particularly in patients who continue high fluid intake despite normalized urinary losses. This complication necessitates patient education regarding appropriate fluid intake and periodic monitoring of serum sodium concentrations, especially during initiation and dose adjustments. Other less common adverse effects include headache, nausea, and hypertension at higher doses. Nephrogenic diabetes insipidus, in contrast, does not respond to vasopressin or desmopressin administration and requires alternative therapeutic approaches including thiazide diuretics, amiloride (for lithium-induced nephrogenic DI), and dietary sodium restriction.

6. Clinical Applications in Critical Care: Vasodilatory Shock

One of the most significant developments in vasopressin pharmacology has been the recognition of its role in managing vasodilatory shock, particularly septic shock. During severe sepsis and septic shock, endogenous vasopressin levels initially increase but subsequently decrease to inappropriately low levels despite ongoing hypotension, a phenomenon termed "vasopressin deficiency" or "relative vasopressin insufficiency." This paradoxical deficiency may result from depletion of pituitary stores, autonomic dysfunction, or enhanced clearance, and contributes to the profound vasodilation and catecholamine resistance characteristic of septic shock.

The rationale for vasopressin supplementation in septic shock derives from multiple mechanisms. First, exogenous vasopressin can restore normal circulating levels, correcting the relative deficiency. Second, the V1a receptor-mediated vasoconstriction occurs through a mechanism distinct from adrenergic receptors, potentially overcoming catecholamine resistance. Third, vasopressin may inhibit ATP-sensitive potassium channels in vascular smooth muscle and reduce production of vasodilatory mediators including nitric oxide. Fourth, vasopressin demonstrates selective vasoconstriction of vessels in splanchnic, renal, and cutaneous beds while relatively sparing coronary, cerebral, and pulmonary circulations, a property that may provide hemodynamic advantages.

The landmark Vasopressin and Septic Shock Trial (VASST), published in 2008, evaluated low-dose vasopressin (0.03 units/minute) versus norepinephrine in patients with septic shock already receiving norepinephrine. While the primary endpoint of 28-day mortality did not differ significantly between groups (35.4% with vasopressin versus 39.3% with norepinephrine, p=0.26), prespecified subgroup analysis demonstrated reduced mortality in patients with less severe shock (defined as norepinephrine requirement less than 15 micrograms/minute). Additionally, vasopressin treatment resulted in decreased requirements for renal replacement therapy, suggesting potential renal protective effects.

Current clinical practice guidelines, including the Surviving Sepsis Campaign, recommend considering vasopressin (at doses up to 0.03 units/minute) as an adjunctive therapy to norepinephrine in patients with septic shock requiring escalating doses of catecholamines. The hormone is typically administered as a fixed-dose infusion rather than titrated to blood pressure, distinguishing it from catecholamine management. Important considerations include the potential for digital and mesenteric ischemia at higher doses, hyponatremia due to antidiuretic effects, and the lack of benefit (and potential harm) at doses exceeding 0.03-0.04 units/minute. Vasopressin may also be useful in other forms of vasodilatory shock including postcardiotomy vasodilatory shock and refractory hypotension during general anesthesia.

7. Hemostatic Applications: Bleeding Disorders

Desmopressin has established efficacy in managing various bleeding disorders, particularly mild hemophilia A and von Willebrand disease (VWD), through mechanisms involving release of coagulation factors from endothelial storage sites. The hormone stimulates endothelial cells to release von Willebrand factor (VWF) and factor VIII from Weibel-Palade bodies into the circulation, transiently increasing plasma concentrations of these factors two- to five-fold within 30-60 minutes of administration. This effect is mediated primarily through V2 receptors on endothelial cells, though V1a receptors may also contribute.

In mild hemophilia A (factor VIII levels 5-30% of normal), desmopressin can elevate factor VIII concentrations sufficiently to achieve hemostasis for minor surgical procedures or bleeding episodes, potentially avoiding the need for factor VIII concentrates. The response shows considerable inter-individual variability, necessitating trial administration prior to planned surgery to assess individual responsiveness. Typical dosing involves 0.3 micrograms/kg administered intravenously over 15-30 minutes or 300 micrograms intranasally.

For von Willebrand disease, desmopressin efficacy depends on disease subtype. Patients with type 1 VWD (partial quantitative VWF deficiency) typically respond well, with most achieving adequate hemostatic levels. Type 2A VWD patients may show variable responses, while type 2B VWD represents a contraindication because desmopressin can precipitate thrombocytopenia by causing platelet aggregation. Type 3 VWD (complete VWF deficiency) does not respond to desmopressin as there are no endothelial VWF stores to release. Consequently, determining VWD subtype is essential before desmopressin administration.

Additional hemostatic applications include prophylaxis for dental procedures in patients with inherited or acquired bleeding tendencies, management of uremic bleeding (where desmopressin may improve platelet function), and reduction of surgical blood loss in patients with normal coagulation undergoing major surgery. Important adverse effects in hemostatic applications include hyponatremia (particularly with repeated dosing), fluid retention, facial flushing, headache, and rarely, arterial thrombotic events in elderly patients or those with cardiovascular disease. Tachyphylaxis develops with repeated administrations due to depletion of endothelial stores, limiting usefulness for sustained therapy.

8. Emerging Therapeutic Applications and Novel Analogues

Contemporary research continues to expand the therapeutic landscape of vasopressin pharmacology through development of selective receptor agonists and antagonists (vaptans) with novel clinical applications. Vasopressin receptor antagonists have emerged as important treatments for conditions characterized by excessive vasopressin activity or water retention, particularly hyponatremia and polycystic kidney disease.

Tolvaptan, a selective V2 receptor antagonist (or "aquaretic"), has been approved for treating hypervolemic and euvolemic hyponatremia in conditions including syndrome of inappropriate antidiuretic hormone secretion (SIADH), heart failure, and cirrhosis. By blocking V2 receptors in the collecting duct, tolvaptan promotes aquaresis (solute-sparing water excretion) without the electrolyte disturbances associated with traditional diuretics. The drug has also gained approval for slowing kidney function decline in autosomal dominant polycystic kidney disease (ADPKD), based on evidence that V2 receptor blockade reduces cystic fluid accumulation and kidney growth. However, hepatotoxicity concerns have necessitated careful monitoring and restricted use in ADPKD to patients at high risk of rapid progression.

Conivaptan, a combined V1a/V2 receptor antagonist available for intravenous use, provides an alternative for hospitalized patients with hypervolemic or euvolemic hyponatremia. The dual receptor blockade may offer advantages in heart failure by combining aquaresis with afterload reduction through V1a-mediated vasodilation. However, widespread use has been limited by administration requirements (continuous infusion), drug interactions (potent CYP3A4 inhibition), and adverse effects including infusion site reactions.

Selepressin, a novel selective V1a receptor agonist under investigation for septic shock, demonstrates enhanced V1a selectivity compared to vasopressin while lacking antidiuretic activity, potentially reducing hyponatremia risk. Phase II and III trials have evaluated whether this improved receptor selectivity profile translates to superior clinical outcomes compared to standard vasopressin, though definitive results regarding mortality benefit remain under investigation.

Central nervous system applications represent another frontier in vasopressin pharmacology. Research has implicated the vasopressin system in social behavior, pair bonding, aggression, and stress responses, prompting investigation of vasopressin-based therapeutics for autism spectrum disorders, social anxiety, and post-traumatic stress disorder. V1a receptor antagonists have shown promise in preclinical models for reducing anxiety-like behaviors and ameliorating social deficits. However, translation to clinical efficacy has proven challenging, and no vasopressin-based therapies have yet achieved regulatory approval for psychiatric indications.

9. Adverse Effects, Contraindications, and Safety Considerations

The adverse effect profile of vasopressin and its analogues varies depending on the specific agent, dose, route of administration, and clinical indication. Understanding these safety considerations is essential for optimizing therapeutic outcomes and minimizing complications.

For therapeutic vasopressin infusions used in vasodilatory shock, the most significant concerns involve excessive vasoconstriction leading to tissue ischemia. Digital ischemia, manifesting as pallor or cyanosis of fingers or toes, has been reported, particularly at doses exceeding recommended levels or in patients with peripheral vascular disease. Mesenteric ischemia represents a more serious complication that can progress to bowel infarction if unrecognized. Myocardial ischemia may occur, particularly in patients with underlying coronary artery disease, due to increased myocardial oxygen demand from elevated afterload combined with potential coronary vasoconstriction. The risk of these ischemic complications increases substantially at vasopressin infusion rates above 0.04 units/minute, explaining current recommendations to limit doses to 0.03 units/minute in septic shock.

Hyponatremia and water intoxication represent the principal risks of desmopressin therapy for diabetes insipidus or bleeding disorders, particularly when fluid intake exceeds output due to excessive antidiuresis. Severe hyponatremia can cause neurological symptoms ranging from headache and nausea to seizures and cerebral edema. Risk factors include excessive fluid consumption, elderly age, use of medications that impair water excretion (thiazide diuretics, selective serotonin reuptake inhibitors), and underlying conditions predisposing to hyponatremia. Preventive strategies include patient education regarding appropriate fluid restriction, avoiding administration before sleep when unconscious fluid intake is minimized, and regular sodium monitoring, especially during treatment initiation and dose adjustments.

Cardiovascular adverse effects of vasopressin and desmopressin include hypertension (more common with vasopressin due to V1a activity), reflex bradycardia, and rarely, arterial thrombotic events including myocardial infarction and stroke. These complications occur more frequently in elderly patients and those with pre-existing cardiovascular disease. Desmopressin's greater V2 selectivity results in less pronounced cardiovascular effects compared to vasopressin, but is not without risk, particularly at higher doses.

Contraindications to vasopressin therapy include known hypersensitivity to vasopressin or its components, though this is rare. For desmopressin specifically, contraindications include moderate to severe renal impairment (due to increased hyponatremia risk), hyponatremia, and, in the context of hemostatic use, type 2B von Willebrand disease (due to thrombocytopenia risk). Relative contraindications include cardiovascular disease (coronary artery disease, heart failure, uncontrolled hypertension), conditions with fluid or electrolyte imbalance, and polydipsia. Vasopressin receptor antagonists are contraindicated in hypovolemic hyponatremia, anuric renal failure, and situations where rapid sodium correction would be dangerous (chronic severe hyponatremia where overly rapid correction risks osmotic demyelination syndrome).

10. Future Directions and Research Perspectives

The vasopressin field continues to evolve with multiple promising research directions that may expand therapeutic applications and improve clinical outcomes. Understanding the complex interplay between vasopressin and other neuroendocrine systems, developing more selective receptor ligands, and identifying biomarkers for treatment response represent key areas of ongoing investigation.

Personalized medicine approaches to vasopressin therapy in septic shock represent an active research area. Current evidence suggests that not all patients with septic shock benefit equally from vasopressin supplementation, with variables such as baseline vasopressin levels, severity of shock, time course of sepsis, and underlying cardiovascular function potentially influencing treatment response. Identifying biomarkers that predict vasopressin responsiveness could enable targeted therapy for patients most likely to benefit. Copeptin, the C-terminal portion of the vasopressin precursor peptide released in equimolar amounts with vasopressin but more stable in circulation, has emerged as a potential biomarker for assessing vasopressin system activation and predicting outcomes in various conditions including sepsis, heart failure, and acute coronary syndromes.

Novel drug delivery systems for vasopressin and analogues may improve therapeutic outcomes and patient convenience. Long-acting formulations of desmopressin, including sustained-release oral preparations and prolonged-duration intranasal formulations, could reduce dosing frequency and improve adherence in diabetes insipidus patients. Sublingual desmopressin formulations have been developed to bypass hepatic first-pass metabolism and reduce inter-individual pharmacokinetic variability. For critical care applications, investigation of automated closed-loop vasopressin infusion systems responsive to real-time hemodynamic parameters could optimize dosing while minimizing adverse effects.

The role of vasopressin in neurodegenerative diseases represents an emerging research frontier. Alterations in vasopressin signaling have been implicated in Alzheimer's disease pathophysiology, with studies suggesting that V1a receptor activation may modulate amyloid-beta production and tau phosphorylation. Investigation of whether vasopressin-based therapies might influence cognitive decline or disease progression in Alzheimer's disease is ongoing. Similarly, the hormone's involvement in sleep regulation and circadian rhythms has prompted exploration of vasopressin system dysfunction in sleep disorders and the potential for chronotherapeutic approaches to treatment.

Genetic approaches to understanding individual variability in vasopressin system function continue to yield insights. Polymorphisms in vasopressin receptor genes have been associated with various phenotypes including social behavior, stress responsiveness, and cardiovascular regulation. Understanding these genetic determinants may enable pharmacogenomic approaches to predicting treatment response and adverse effects. Gene therapy approaches to restore vasopressin production in central diabetes insipidus, while still experimental, represent a potential future alternative to lifelong pharmacological replacement.

Environmental and societal applications of vasopressin research extend beyond traditional medical therapeutics. Understanding the hormone's role in social bonding, aggression, and parental behavior has implications for understanding human social dynamics and potentially developing interventions for social dysfunction. The vasopressin system's involvement in stress responses and emotional regulation continues to be explored in the context of post-traumatic stress disorder, anxiety disorders, and depression, though translation to approved therapeutics has been elusive.

Conclusion

Vasopressin represents a paradigmatic hormone whose study has illuminated fundamental principles of neuroendocrine physiology, receptor pharmacology, and homeostatic regulation. From its initial discovery over a century ago to contemporary applications in critical care medicine and emerging roles in neuroscience, vasopressin research continues to generate insights with broad clinical implications. The hormone's essential functions in osmoregulation and fluid balance, mediated primarily through V2 receptors in the kidney, underpin the successful treatment of diabetes insipidus with desmopressin. The recognition of vasopressin's role in vasodilatory shock and the development of low-dose vasopressin therapy for septic shock represent major advances in critical care medicine, potentially improving outcomes in one of medicine's most challenging conditions.

The development of selective vasopressin receptor agonists and antagonists has expanded therapeutic possibilities, enabling targeted interventions for conditions ranging from hyponatremia to polycystic kidney disease to bleeding disorders. Understanding the distinct signaling mechanisms and tissue distributions of V1a, V1b, and V2 receptors has been crucial to these advances, demonstrating the power of molecular pharmacology to drive therapeutic innovation. Ongoing research into novel vasopressin analogues with enhanced selectivity, prolonged duration of action, or improved safety profiles promises to further expand the clinical utility of this important drug class.

Looking forward, the integration of vasopressin pharmacology with advances in biomarker development, pharmacogenomics, drug delivery technology, and systems biology approaches to complex disease holds promise for more precise, personalized therapeutic applications. The hormone's involvement in diverse physiological processes from cardiovascular regulation to social behavior to circadian rhythms ensures that vasopressin will remain an active and productive area of investigation. As our understanding of vasopressin's multifaceted roles continues to deepen, new therapeutic opportunities will likely emerge, building on the strong foundation established by decades of rigorous basic and clinical research. The vasopressin story exemplifies how thorough understanding of a molecule's biology, from gene to receptor to physiological function, can illuminate disease pathophysiology and generate therapeutic approaches that significantly impact patient care across multiple medical disciplines.

This literature review was prepared for biotechpharma.org
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