Evidence mapPaperPMID 42379375Full record

ArticleJournal of lipid research2026

BK channel deficiency promotes lipolysis via an AKT-independent activation of the cAMP/PKA/HSL pathway.

Jin Zhang, Xin Shi, Mengxuan Zhang, Yuying Han, Guang Yang, Ruiyang Li, Feng Zhao, Ping Liu, Xinxin Wen, Wenxuan Wei and 7 more

Abstract read
In one paragraph

Article in Journal of lipid research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Jin ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China; Central Laboratory, Beijing Luhe Hospital, Capital Medical University, Beijing, People's Republic of China.
Xin ShiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Mengxuan ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Yuying HanDepartment of Medical Genetics and Developmental Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Guang YangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Ruiyang LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Feng ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Ping LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China; Beijing Lab for Cardiovascular Precision Medicine, Beijing, People's Republic of China; Laboratory for Clinical Medicine, Capital Medical University, Beijing, People's Republic of China.
Xinxin WenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China; Laboratory for Clinical Medicine, Capital Medical University, Beijing, People's Republic of China.
Wenxuan WeiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Bojing ZuoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Biao ZhengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Hongshan LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Wenjing LuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China.
Meili WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China; Beijing Lab for Cardiovascular Precision Medicine, Beijing, People's Republic of China.
Zhifei ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China. Electronic address: Zhifeiz@ccmu.edu.cn.
Haixia HuangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China; Beijing Lab for Cardiovascular Precision Medicine, Beijing, People's Republic of China; Laboratory for Clinical Medicine, Capital Medical University, Beijing, People's Republic of China. Electronic address: haixiah@ccmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipocyte lipolysis mobilizes stored triglycerides during energy deprivation, a process tightly regulated to maintain metabolic homeostasis. The large conductance calcium-activated potassium channel (BK) is present in adipocytes and is involved in intracellular lipid metabolism. This study aims to investigate the role of BK in regulating adipocyte lipolysis. Using BK knockout (BK-KO) rats, adipocyte-specific BK knockout (BK

Indexed as

adipocytesBK channelscAMP/PKA/HSL pathwaylipolysisobesity

Identifiers

PMID42379375
PMCPMC13430265

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.