Of Mice and Men and Plethysmography Systems : Does LKB1 Determine the Set Point of Carotid Body Chemosensitivity and the Hypoxic Ventilatory Response?
© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG..
Our recent studies suggest that the level of liver kinase B1 (LKB1) expression in some way determines carotid body afferent discharge during hypoxia and to a lesser extent during hypercapnia. In short, phosphorylation by LKB1 of an as yet unidentified target(s) determines a set point for carotid body chemosensitivity. LKB1 is the principal kinase that activates the AMP-activated protein kinase (AMPK) during metabolic stresses, but conditional deletion of AMPK in catecholaminergic cells, including therein carotid body type I cells, has little or no effect on carotid body responses to hypoxia or hypercapnia. With AMPK excluded, the most likely target of LKB1 is one or other of the 12 AMPK-related kinases, which are constitutively phosphorylated by LKB1 and, in general, regulate gene expression. By contrast, the hypoxic ventilatory response is attenuated by either LKB1 or AMPK deletion in catecholaminergic cells, precipitating hypoventilation and apnea during hypoxia rather than hyperventilation. Moreover, LKB1, but not AMPK, deficiency causes Cheyne-Stokes-like breathing. This chapter will explore further the possible mechanisms that determine these outcomes.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:1427 |
|---|---|
| Enthalten in: |
Advances in experimental medicine and biology - 1427(2023) vom: 28., Seite 163-173 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Evans, A Mark [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 19.06.2023 Date Revised 13.03.2024 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.1007/978-3-031-32371-3_18 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM358239346 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM358239346 | ||
| 003 | DE-627 | ||
| 005 | 20240313233502.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1007/978-3-031-32371-3_18 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1326.xml |
| 035 | |a (DE-627)NLM358239346 | ||
| 035 | |a (NLM)37322347 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Evans, A Mark |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Of Mice and Men and Plethysmography Systems |b Does LKB1 Determine the Set Point of Carotid Body Chemosensitivity and the Hypoxic Ventilatory Response? |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 19.06.2023 | ||
| 500 | |a Date Revised 13.03.2024 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG. | ||
| 520 | |a Our recent studies suggest that the level of liver kinase B1 (LKB1) expression in some way determines carotid body afferent discharge during hypoxia and to a lesser extent during hypercapnia. In short, phosphorylation by LKB1 of an as yet unidentified target(s) determines a set point for carotid body chemosensitivity. LKB1 is the principal kinase that activates the AMP-activated protein kinase (AMPK) during metabolic stresses, but conditional deletion of AMPK in catecholaminergic cells, including therein carotid body type I cells, has little or no effect on carotid body responses to hypoxia or hypercapnia. With AMPK excluded, the most likely target of LKB1 is one or other of the 12 AMPK-related kinases, which are constitutively phosphorylated by LKB1 and, in general, regulate gene expression. By contrast, the hypoxic ventilatory response is attenuated by either LKB1 or AMPK deletion in catecholaminergic cells, precipitating hypoventilation and apnea during hypoxia rather than hyperventilation. Moreover, LKB1, but not AMPK, deficiency causes Cheyne-Stokes-like breathing. This chapter will explore further the possible mechanisms that determine these outcomes | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a AMPK | |
| 650 | 4 | |a AMPK related kinases | |
| 650 | 4 | |a Brainstem | |
| 650 | 4 | |a Carotid body | |
| 650 | 4 | |a Hypoxia | |
| 650 | 4 | |a Hypoxic ventilatory response | |
| 650 | 4 | |a LKB1 | |
| 650 | 4 | |a Mitochondria | |
| 650 | 7 | |a Protein Serine-Threonine Kinases |2 NLM | |
| 650 | 7 | |a EC 2.7.11.1 |2 NLM | |
| 650 | 7 | |a AMP-Activated Protein Kinases |2 NLM | |
| 650 | 7 | |a EC 2.7.11.31 |2 NLM | |
| 773 | 0 | 8 | |i Enthalten in |t Advances in experimental medicine and biology |d 1971 |g 1427(2023) vom: 28., Seite 163-173 |w (DE-627)NLM000012157 |x 0065-2598 |7 nnns |
| 773 | 1 | 8 | |g volume:1427 |g year:2023 |g day:28 |g pages:163-173 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1007/978-3-031-32371-3_18 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 1427 |j 2023 |b 28 |h 163-173 | ||