What is the clinical evidence from this study?

Study design: Other. Population: Age-induced cardiac dysfunction. Intervention: CLPB knockdown (AAV9-sh-CLPB) vs. SAMP8-GFP mice and SAMR1 control mice. Primary outcome: Cardiac function (ejection fraction and fractional shortening) and mitochondrial function.

What type of study is this?

This is a Cohort Study study (also classified as: Experimental Study).

October 10, 2025Circulation Research

Abstract Wed018: Modulating mitochondrial protein quality control in age-induced cardiac dysfunction

View Full Paper

Ask AI

Bookmark

Key result

CLPB knockdown mitigates age-related cardiac dysfunction and improves LVEF in aging mice.

Why the study?

Does CLPB knockdown improve mitochondrial and cardiac function in aging mouse models?

Population

Senescence-accelerated prone 8 mice and senescence-accelerated mouse resistant 1 control mice; in vitro…

Comparison

AAV9-cTNT-CLPB and AAV9-sh-CLPB vs Control mice (SAMR1) and SAMP8-GFP mice

Design

Preclinical

Follow-up

Evaluated at 3, 6, and 9 months of age

Authors

SKShiridhar KashyapWake Forest University AKAshlesha KadamWake Forest University SSShatakshi ShuklaMaharaja Sayajirao University of Baroda

Discussion

Member takes

Implication

Knockdown of the mitochondrial chaperonin CLPB mitigates age-induced mitochondrial and cardiac dysfunction in a preclinical mouse model of aging.

Key Points

CLPB loss improved mitochondrial function and cardiac performance in aging SAMP8 mice and doxorubicin-treated HL-1 cells.
Echocardiographic assessments indicated enhanced ejection fraction in CLPB knockout mice compared to controls.
Mitochondrial chaperonin CLPB shows age-dependent expression reduction in SAMP8 mice, linking it to heart disease.
Doxorubicin treatment in HL-1 cells confirmed CLPB's role in moderating ROS levels and maintaining mitochondrial integrity.

Structured PICO

Does CLPB knockdown improve mitochondrial and cardiac function in aging mouse models?

Population

In vivo aging mouse models (SAMP8) and in vitro mouse cardiac cells (HL-1) evaluated for age-induced and doxorubicin-induced cardiac and mitochondrial dysfunction.

Intervention

AAV9-cTNT-CLPB (overexpression model) and AAV9-sh-CLPB (knockdown model)

Comparator

Control mice (SAMR1) and SAMP8-GFP mice

Outcome

Cardiac function (ejection fraction, fractional shortening) and mitochondrial function (respiration, calcium retention capacity, ROS levels, membrane potential, oxygen consumption rate)surrogate

Knockdown of the mitochondrial chaperonin CLPB mitigates age-induced mitochondrial and cardiac dysfunction in a preclinical mouse model of aging.

Cite This Study

Kashyap et al. (2025) studied Age-induced cardiac dysfunction. CLPB knockdown (AAV9-sh-CLPB) vs. SAMP8-GFP mice and SAMR1 control mice was evaluated on Cardiac function (ejection fraction and fractional shortening) and mitochondrial function. Loss of CLPB mitigated age-induced mitochondrial and cardiac dysfunction, improving ejection fraction and fractional shortening in aging mice.

synapsesocial.com/papers/68e861a57ef2f04ca37e47cd https://doi.org/10.1161/res.137.suppl_1.wed018

View Full Paper

Ask AI

Bookmark

Implication

Knockdown of the mitochondrial chaperonin CLPB mitigates age-induced mitochondrial and cardiac dysfunction in a preclinical mouse model of aging.

Abstract Wed018: Modulating mitochondrial protein quality control in age-induced cardiac dysfunction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Abstract Wed018: Modulating mitochondrial protein quality control in age-induced cardiac dysfunction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider