Table 1.

Some phenomena of cellular stress characterizing possible stages of its development.

Phenomena	Stage 1	Stage 2	Stage 3
Proliferation	activated	variable	suppressed
Dominance 1 of growth factors	yes	no	no
Insulin resistance	no	possible	yes
Phosphoinositide 3-kinases (PI3K) 2	activation	not typical	not typical
mTORC1 expression	high	variable	variable or low
Autophagy	low	elevated	high
Inflammasomes	low	NLRP3 activation in various cells
Apoptosis	possible	possible	possible
Programmed necrosis 3	not typical	unlikely	possible
Effects of SR on PRR	suppressed	variable	activated
Purinergic receptors 4	P1	P2X and P2Y	P2X and P2Y
p53/NF-κB ratio	↑/↓	↓/↑	↓/↑
Mitogen activated protein kinases	ERK > JNK and p38	ERK < JNK and p38	ERK < JNK and p38
Production and reception of pro-inflammatory cytokines	moderate	high	Unstable 4
iNOS endotheliocytes	inactive	inactive	active
cNOS endotheliocytes	?	inhibited	?
Unfolded protein response	progression
ROS formation	progression
NF-κB, AP-1, HIF-1α, HSFs, Egr	progression of expression of these transcription factors
The role of non-coding RNA	depends on cell type and formation of extracellular vesicles

Note: It is the author’s integral table compiled as a result of the analysis of numerous literature data presented in the text of Section 2.5. ¹—in the cytokine spectrum; ²—PI3K, which is dependent on insulin and many growth factors; ³—pyroptosis, necroptosis, NETosis, autophagic cell death; ⁴—main ligands: for P1—adenosine, for P2—ATP; ↑/↓—more/less; SR—scavenger receptor; PRR—pattern recognition receptor; ROS—reactive oxygen species; NOS—NO synthase: i—inducible and c—constitutive.