Evidence map›Paper›PMID 37670891›Full record

ReviewFrontiers in endocrinology2023

New therapeutic directions in type II diabetes and its complications: mitochondrial dynamics.

Shengnan Wang, Haiyang Zhao, Suxian Lin, Yang Lv, Yue Lin, Yinai Liu, Renyi Peng, Huanzhi Jin

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
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

28 citing papers in PubMed, 28 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Shengnan WangDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Haiyang ZhaoInstitute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang, College of Life and Environmental Science, Wenzhou University, Wenzhou, China.
Suxian LinDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Yang LvDepartment of Rheumatology and Immunology, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Yue LinGeneral Practitioner, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Yinai LiuInstitute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang, College of Life and Environmental Science, Wenzhou University, Wenzhou, China.
Renyi PengInstitute of Life Sciences & Biomedicine Collaborative Innovation Center of Zhejiang, College of Life and Environmental Science, Wenzhou University, Wenzhou, China.
Huanzhi JinGeneral Practitioner, The Third Affiliated Hospital of Shanghai University, Wenzhou No.3 Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Wenzhou Medical University · CNWenzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and optic atrophy 1 (Opa1), and the latter is mediated by dynamin related protein 1 (Drp1), mitochondrial fission 1 (Fis1) and mitochondrial fission factor (MFF). Mitochondrial fusion and fission are generally in dynamic balance and this balance is important to preserve the proper mitochondrial morphology, function and distribution. Diabetic conditions lead to disturbances in mitochondrial dynamics, which in return causes a series of abnormalities in metabolism, including decreased bioenergy production, excessive production of reactive oxygen species (ROS), defective mitophagy and apoptosis, which are ultimately closely linked to multiple chronic complications of diabetes. Multiple researches have shown that the incidence of diabetic complications is connected with increased mitochondrial fission, for example, there is an excessive mitochondrial fission and impaired mitochondrial fusion in diabetic cardiomyocytes, and that the development of cardiac dysfunction induced by diabetes can be attenuated by inhibiting mitochondrial fission. Therefore, targeting the restoration of mitochondrial dynamics would be a promising therapeutic target within type II diabetes (T2D) and its complications. The molecular approaches to mitochondrial dynamics, their impairment in the context of T2D and its complications, and pharmacological approaches targeting mitochondrial dynamics are discussed in this review and promise benefits for the therapy of T2D and its comorbidities.

Indexed as

Diabetes Mellitus, Type 2ApoptosisHomeostasisHumansMitochondriaMitochondrial Dynamicsdiabetic complicationsmitochondrial dynamicsmitochondrial fissionmitochondrial fusiontype II diabetes

Identifiers

PMID37670891
PMCPMC10475949
OpenAlexW4386033442

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.