Table 1 Genes potentially involved in the pathophysiology of asthma and hypertension, according to literature published before 2018.

TLR4

pathogen recognition and activation of innate immunity

Up-regulated in lungs of spontaneously hypertensive rats (SHR) compared to normotensive ancestor strain (WKY rats) in response to combustion source particulate matter treatment which irritates lungs⁹⁶

CXCL2 (MIP-2)

suppress hematopoietic progenitor cell proliferation

CD14

mediates the innate immune response to bacterial lipopolysaccharides

RHOA

reorganization of the actin cytoskeleton and regulation of cell shape, attachment, and motility

Up-regulated in rodent models of asthma and hypertension; inhibition leads to improvement of both conditions⁹⁷. ROCK inhibitors suppress smooth muscle contraction and may treat arterial hypertension and asthma⁹⁸

ROCK1

regulates formation of focal adhesions

GNA12, GNA13

signal transduction

These genes encode G-protein subunits transducing the signal from activated GPCR to RhoGEFs activating RHOA. Abnormal G12/13 signaling is involved in the pathogenesis of arterial hypertension and bronchial asthma, among other pathophysiological conditions⁹⁹

SLC26A4

encodes transmembrane anion exchanger

Madeo et al.¹⁰⁰ reported a variant of SLC26A4 with potentially protective effect for both asthma and hypertension

ADRB1, ADRB2

mediate the physiological effects of the epinephrine and norepinephrine

These genes encode proteins targeted by drugs used against asthma and hypertension; some variants are associated with response to anti-hypertensive¹⁰¹ anti-asthmatic therapy¹⁰²