Major human receptor families: types and functions.
| Receptor family[primary location] | Number of types/Subtypes | Primary function | Survival-critical? | Loss consequences | Redundancy level |
|---|---|---|---|---|---|
| G protein-coupled receptors (GPCRs)[cell membranes (widespread)] | 367 | Sensory, cognitive, metabolic, immune signaling [63–65]. | Some (e.g., β1-AR) [66] | Cardiac failure (e.g., β1-AR knockout) [66] | High |
| Adrenergic receptors[sympathetic nervous system, heart, vasculature] | 9 (α1A/B/D, α2A/B/C, β1, β2, β3) | Regulation of cardiovascular tone, cardiac output, vascular resistance, and metabolic mobilization [66]. | Yes (β1-AR) [66] | Severe bradycardia, impaired cardiac contractility, heart failure [66] | Moderate (partial cross-compensation among α/β subtypes) |
| Serotonin (5-HT) receptors[CNS, GI tract, vasculature] | 14 | Mood, cognition, GI, vascular tone [67]. | Yes (5-HT2C) [83] | Seizure susceptibility, early death [83] | Low |
| Cannabinoid receptors[CNS, immune system] | 2 | Neuromodulation, immune regulation [68]. | No | Altered immune/neurologic tone [68] | High |
| Olfactory receptors[odorant detection chemosensation] | Hundreds | Sensory; expressed in non-olfactory tissues [69]. | No | Sensory loss only [69] | High |
| Nuclear receptors (e.g., GRα, MR, PPARs, ER, AR, TR, VDR)[nucleus (widespread)] | 48 | Ligand-activated transcriptional regulators controlling metabolism, development, and inflammation [70]. | Yes (GRα, MR) [58, 83] | GRα: multisystem failure; MR: salt wasting, vascular collapse [58, 84] | GRα: none; MR: low |
| Receptor tyrosine kinases (RTKs)[cell membranes of endocrine, metabolic, and growth-regulated tissues] | ~20 families (e.g., insulin, IGF-1, EGF, VEGF receptors) | Regulate cell growth, metabolism, differentiation, and survival via phosphorylation cascades (e.g., MAPK, PI3K/Akt). | Yes (insulin receptor) | Neonatal hypoglycemia, metabolic failure, impaired growth | Low to moderate |
| Ligand-gated ion channel receptors (ionotropic)[neuronal membranes] | Various | Fast neurotransmission, neuromuscular signaling [71]. | Yes (e.g., NMDA) [92] | Neuronal apoptosis, early lethality [92] | Low to moderate |
| NMDA receptors[CNS (synapses)] | Multiple | Synaptic plasticity, learning, neurodevelopment [92, 93]. | Yes [92] | Neurodegeneration, perinatal lethality [92] | Low |
| Sensory receptors[skin, eyes, ears, viscera] | Multiple | Detection of internal and external stimuli [72]. | No | Impaired sensory perception [72] | High |
| T cell receptors (TCRs)[T lymphocytes] | Millions | Adaptive immunity, antigen recognition [73]. | No | Immunodeficiency [73] | High |
| Toll-like receptors (TLRs)[macrophages, dendritic cells] | ~10 | Innate immunity, pathogen recognition [74]. | No | Impaired innate response [74] | High |
| TREMs[several] | Several | immune regulation, inflammation control [75]. | No | Impaired inflammation regulation [75] | High |
| Cytokine receptors (e.g., IL-1R, IL-2R, TNFR)[Immune and epithelial cells] | Many | Immune activation, inflammation, cell survival [76]. | No | Dysregulated immunity [76] | High |
| Adenosine receptors (P1 purinergic, GPCR subclass)[CNS, vasculature, immune cells] | Multiple | Pain modulation, immune, vascular tone [77]. | No | Reduced nociception, altered perfusion [77] | High |
| Neuropeptide Y receptors—GPCR subclass | Y1–Y3 | Appetite, stress response, circadian rhythms [78]. | No | Metabolic dysregulation [78] | High |
| Presynaptic GPCR (e.g., GABAB, 5-HT1B)[presynaptic terminal in CNS] | Various | Neurotransmitter feedback regulation [79]. | No | Altered synaptic signaling [79] | High |
| Angiotensin receptors, GPCR subclass[kidneys, vasculature, brain] | AT1, AT2 | Cardiovascular, renal, CNS function [80]. | No | Hypertension, metabolic shifts [80] | Moderate |
| Common γ-chain (CD132, IL-2RG subunit)[lymphoid tissues] | Shared subunit | Lymphocyte development; shared component of IL-2, IL-4, IL-7, IL-9, IL-15, IL-21 receptor complexes [81]. | Yes [81] | Severe combined immunodeficiency [81] | None |
| KISS1R (kisspeptin receptor, GPCR subclass)[hypothalamus] | Single | Regulate reproductive axis activation and puberty [82]. | No | Infertility, delayed puberty [82] | Moderate |
This table categorizes major receptor families in the human body by structural classification, number of subtypes, physiological location, primary functions, and relevance to survival and redundancy. Receptors are grouped into membrane-bound (e.g., GPCRs, ionotropic channels), cytoplasmic, and nuclear families, reflecting their distinct yet coordinated roles in cellular signaling and systemic regulation. The “number of types/subtypes” column denotes recognized functional isoforms. The “primary location” and “primary function” columns summarize tissue distribution and physiological role. AR: androgen receptor; CNS: central nervous system; ER: estrogen receptor; GI: gastrointestinal; GRα: glucocorticoid receptor alpha; IGF-1: insulin-like growth factor 1; IL-1R: interleukin-1 receptor; IL-2R: interleukin-2 receptor; IL-2RG: interleukin-2 receptor gamma chain; NMDA: N-methyl-D-aspartate; KISS1R: kisspeptin receptor; MR: mineralocorticoid receptor; PPARs: peroxisome proliferator-activated receptors; TREMs: triggering receptor expressed on myeloid cells; TR: thyroid hormone receptor; TNFR: tumor necrosis factor receptor; VDR: vitamin D receptor; VEGF: vascular endothelial growth factor.
This work is dedicated to Professor George P. Chrousos’s guidance and mentorship over the past twenty years and to Don Donati, Esq., for his steadfast support of academic freedom and research integrity.
AI-Assisted Work Statement: The content of Table 1 was synthesized from structured evidence obtained via the Consensus research platform and organized with editorial assistance from ChatGPT (OpenAI) to ensure clarity, consistency, and accurate citation. Preparation of the comparative analysis of Tables 2 and 3 was supported by insights derived from Consensus (https://consensus.app), a PubMed-linked AI research synthesis platform used to verify and update biomedical references, and ChatGPT (GPT-5, OpenAI, 2025), which assisted in drafting and formatting the table, integrating reference alignment, and refining academic clarity. Both tools were used exclusively to enhance scientific precision and presentation quality; all final interpretations and conclusions reflect the author’s independent critical analysis. After using the tool/service, author(s) reviewed and edited the content as needed and take(s) full responsibility for the content of the publication.
GUM: Conceptualization, Investigation, Methodology, Writing—original draft, Project administration, Writing—review & editing. The author read and approved the submitted version.
The author has no competing interests to declare or any real or perceived financial interest in any product or commodity mentioned in this paper.
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